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C.F. Burgoyne, J.C. Downs, A. Bellezza, L. Wang, B. Fortune, G. Cull, G.A. Cioffi; Axon Loss at the Onset of Confocal Scanning Laser Tomographic (CSLT) Detected Optic Nerve Head (ONH) Surface Change in Early Experimental Glaucoma (EEG) Is Modest (16–29%) and Diffuse (Central and Peripheral) . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2372.
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Purpose: Profound deformation of the lamina cribrosa , neural canal and peripapillary sclera are present in EEG (Burgoyne, et al, IOVS, 2004; 45:4378). The purpose of this report is to characterize overall and regional axon loss at this same stage of CSLT–detected, EEG. Methods: Four young adult (8 years old) EEG monkeys (one eye given laser–induced IOP elevation, then followed to the onset of CSLT–detected ONH surface change) and one normal (N) monkey were perfusion–fixed, then both eyes were enucleated, and three cuts (one S and two N) made along the full length of each optic nerve (ON). For each eye, the ON was cut 1 mm posterior to the lamina, sectioned and processed for ON axon counting in 16 regions (8 central, 8 peripheral – Cioffi, et al, Arch Ophthal 2004; 122:1517), while the ONH was trephined, embedded in paraffin, and microtome serial sectioned (from the vitreous, through the lamina and into the ON until at least 2 of the 3 ON cuts were visible), then 3D reconstructed (Burgoyne, et al, IOVS, 2004; 45:4378), and digitally overlayed onto clinical stereophotos to ensure accurate orientation. For each EEG eye, regions of significant (p< 0.01, ANOVA) axon loss (compared to the contralateral N eye) were then compared. Results: Overall axon loss was 16 %,17%, 19% and 29%, and regional axonal difference ranged from +21% to – 41%, in the 4 EEG eyes. Regional axonal difference in the N monkey ranged from –5 to +13 %. In 2 EEG eyes (17 and 19% axon loss – peak detected IOP 25 and 20 mm Hg, duration 2 to 9 weeks) regions of significant axon loss were both central and peripheral without specific patterns but with slight preference to the inferior hemisphere. In the other EEG eyes, (16 and 29% axon loss, peak detected IOP 21 and 37 mm Hg, duration 3.5 and 4.5 weeks), dense, contiguous regional axon loss occurred with overall superior sparing. Conclusions: Axon loss is modest and diffuse and may also be superior sparing and pre–perimetric at the onset of CSLT detected EEG in young adult monkey eyes. Regardless of the mechanism of axonal damage, for a given IOP–related insult, the more–compliant young adult monkey lamina may be more susceptible to early plastic deformation, enabling CSLT–detected EEG to reflect more laminar deformation and less axon loss in the young adult monkey eye. Axon loss at the onset of CSLT–detected EEG in older (less–compliant) monkey eyes will now be studied.
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