How consistent is this observation between the two areas? Does this depend on the type of glaucoma?
Studies have confirmed that chronic IOP elevation causes posterior and lateral displacement of the lamina cribrosa, which results in compression of the axons and disruption of axoplasmic flow. The damage first involves axonal bundles throughout the nerve with somewhat greater involvement of the inferior and superior poles. With continued optic nerve damage, the susceptibility of the polar zones becomes more prominent. In addition, histologic studies of optic nerves indicate that nerve fibers larger than the normal mean diameter atrophy more rapidly in glaucomatous eyes, although no fiber size is spared from damage. This preferential loss of large fibers appears to be due to a higher proportion of the fibers in the inferior and superior poles.
Consequently, early visual loss in glaucoma commonly occurs in the arcuate area, especially in the superior half, which correlates with the predilection of the inferior and superior temporal poles of the optic nerve head for early glaucomatous damage.
The loss of retinal nerve fibers rarely proceeds at the same rate in the upper and lower portions of an eye. Consequently, a step like defect is frequently created where the nerve fibers meet along the median raphe. Because the superior field is involved somewhat more frequently than the inferior portion is in the early stages of glaucoma, the nasal step more often results from a greater defect above the horizontal midline, which is referred to as a superior nasal step. However, inferior nasal steps are not uncommon. [Source of information: Shields’ textbook of glaucoma]
As far as the effect of types of glaucoma and frequency of superior and inferior arcuate field defect are concerned, Phelps et al found in their study that the most frequent defects in both low-tension glaucoma and primary open angle glaucoma were superior nasal defects and superior arcuate scotomas. ( Phelps CD, Hayreh SS, Montague PR: Visual fields in low tension glaucoma, primary open angle glaucoma and anterior ischemic optic neuropathy. Doc Ophthalmol 35:113, 1983)
The other fellows have done a wonderful job in providing confirmation that it is the superior half of the visual field the one that usually gets involved first and that the superior and inferior poles of the optic nerve are more prone to early damage. However, the answer to the question “why the superior visual field goes first?”, remains unanswered.
A good explanation comes from the fact that the foveola does not lie exactly midway between the superior and inferior optic nerve head poles, but slightly inferior. The latter determines that the axons of the lower half of the retina under the raphe crowd together more in the inferior pole of the optic nerve -and thus are more prone to early damage- than those coming from the retina above the raphe, which spread more around the middle (temporal) and superior aspects of the optic nerve, thus achieving less crowding and being less prone to early damage than the axons exiting the globe at the inferior pole. I hope this explanation is useful for you. Hood-DC PhD is a good source and reference for further explanations if needed.
Having looked at LOTS of VFs and LOTS of optic nerve stereoscopic photographs, I can confidently agree that 1) superior VF defects occur first (usually nasal step), more often than inferior defects, and 2) these defects are associated with inferior temporal rim thinning and/or RNFL defects, which are the most common early indicators of GON by photo assessment. Regarding why, I don't really know. The structural idea described above (relative location of the fovea in relation to nerve fiber bundles) may provide a clue.
I agree entirely with Dr. BOWD THAT1) superior VF defects occur first (usually nasal step), more often than inferior defects, and 2) these defects are associated with inferior temporal rim thinning and/or RNFL defects, which are the most common early indicators of GON by photo assessment.
Perhaps this paper might be useful for you:
https://www.researchgate.net/publication/23392738_Standard_automated_perimetry_and_algorithms_for_monitoring_glaucoma_progression?ev=prf_pub
Article Standard automated perimetry and algorithms for monitoring g...
I have different explanation of pathogenesis of arcuate field defects and early loss of inferior arcuate fibers giving rise to superior arcuate defects. Due to sinking of the LC the entire 360 degrees of the nerve fibers are stretched and broken starting with the peripheral fibers and ending with central. All the temporal fibers consisting of macular, superior and inferior arcuate fibers are severed simultaneously. However the arcuate fibers being fewer in number compared to the macular fibers are depleted earlier giving rise arcuate field defects.
Question: why superior arcuate first? For this I propose that the inferior arcuate fibers may be lesser than superior arcuate fibers so depleted earlier than superior arcuate fibers. Severance of the nerve fibers appears to be missing card in glaucoma. The sharply defined arcuate field defects can never be produced by atrophy of nerve fibers. It is hard to believe that certain group of nerve fibers are more sensitive than others I think all the nerve fibers are equally prone to damage. Glaucoma may not be optic disc neuropathy but an axotomy.
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