Abstract
For many years, there has been debate over the mechanism by which elevated intraocular pressure (IOP) damages optic nerve fibers in glaucoma. Damage appears to be initiated at the scierai lamina cribrosa, just in front of the myelin line in the optic nerve head (Anderson and Hendrickson 1974; Minckler et al. 1978; Quigley and Green 1979; Quigley et al. 1981b). Physical rearrangements of the lamina occur early in the glaucoma damage process in human eyes, caused by elevated IOP (Quigley et al. 1981b; Quigley et al. 1982; Quigley et al. 1983b). This compression of the ten successive sheets of the lamina, along with the loss of neural tissue from the disk rim are the reason the disk cup looks deeply excavated in the process we call “cupping”. The stretching and collapse of the lamina cribrosa is greatest at the superior and inferior poles of the nerve head, where the loss of fibers is greater (Quigley and Addicks 1981a; Quigley et al. 1981b; Quigley et al. 1983a).
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References
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© 1987 Springer-Verlag Berlin Heidelberg
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Quigley, H.A. (1987). Optic Nerve Head Blood Flow is Normal in Chronic Experimental Glaucoma. In: Krieglstein, G.K. (eds) Glaucoma Update III. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71785-7_7
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DOI: https://doi.org/10.1007/978-3-642-71785-7_7
Publisher Name: Springer, Berlin, Heidelberg
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