Glaucomatous field defects corroborate with the arrangement of nerve fibers in the retina or of the prelaminar region of the ONH. Superior and inferior arcuate NFs originate at the temporal horizontal raphe, so, when arcuate NFs are destroyed the Ronnie’s nasal step is produced.
But, as the loose prelaminar NFs enter the LC, the arrangement of the NFs changes dramatically. Loose NFs become fastened in bundles in the pores of LC which are not only irregular in size but also irregularly arranged as well. Macular NFs move to occupy the central location, thus the arcuate fibers lose their pattern and get mingled with the rest of temporal fibers. New arrangement of NFs becomes well defined in the optic nerve after the NFs leave the LC.
Question arises: If the NFs are arranged in bundles in the intricate meshwork of irregularly placed pores of LC, then we should expect the glaucomatous field defects to be very irregular as well. But this is not the case since the arcuate field defects have sharp margins and sharply defined nasal step. Therefore, the primary site of injury in glaucoma has to be either retina or the prelaminar area but not the lamina cribrosa.
A very good thought. I think sir, that from the very beginning , our brain is hard wired and familiar to the retinal nerve fibres as illustrated in books in a "en face" pictograph. In a cut section at the level of lamina , i have my own hypothesis /theory- not proven that, the fibres travelling towards the arcuates travel in the outer bundles and to the macula in a more central or inner bundle. At the level of lc, there is a sudden bend. (inner fibres have a more linear curvature while the outer has a more sharp - Contemplating the circular running tracks).Due to the pressure effect, i feel there is an impingement of the fibres in the outer layers as the scleral end ( which have sharper turn/bend- and end up having disturbed axoplasmic flow eariler- (contemplating neuropraxia at microlevel) which in long term - eventually goes into atrophy. as pressure continues to rise and the optic cup increases, other nerve fibre layers are pushed more outwards and towards the rim, causing them to have similar bend and axoplasmic disturbance. In congenital glaucoma, sclera being elastic, if iop is controlled early , the cup size reverses -hence causing the impingement to break and could support the theory of the preserved functionality of the remaining fibres. Probably with better Swept source algorithms and deep range imaging , we may be able to test optic disc head for this theory by testing eyes with specific visual field defects.
What you have stated: may hold true for high-tension glaucoma. How would you theory explain in normal -tension glaucoma?
My hypothesis since 2006 is that lamina cribrosa is sinking (already proven in 2010) with the result prelaminar nerve fibers are being stretched and broken. Glaucoma is not a optic neuropathy but and optic disc axotomy. There is plenty of morphological and histological proof for it. Only thing we have to do is: to look at the glaucoma disc in context of sinking LC and severance of NFs. Smaller vasculature is meeting the same fate resulting in splinter hemorrhages .
Glaucomatous field defects such as arcuate scotoma are horizontally oriented correlating with the arrangement of NFs while in retina. The NFs make a 90-degree turn in the ONH and become vertically oriented in the prelaminar region and LC. After the 90 degree turn there is neither horizontal raphe nor are the arcuate NFs. Therefore, the characteristic glaucomatous field defects such as arcuate scotoma and Ronnie's nasal step can't be produced if injury to NFs occurs after their 90 degree turn and become vertically oriented.
Can any researcher please explain how the arcuate scotoma and Ronnie's nasal step be produced if LC is the site of injury - when no such arrangement is present in LC. Thank you in advance for the answer.
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