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The Morphological Difference Between Glaucoma and Other Optic Neuropathies

Burgoyne, Claude MD

Journal of Neuro-Ophthalmology: September 2015 - Volume 35 - Issue - p S8–S21
doi: 10.1097/WNO.0000000000000289
Original Contribution

Abstract: The clinical phenomenon of cupping has 2 principal pathophysiologic components in all optic neuropathies: prelaminar thinning and laminar deformation. We define prelaminar thinning to be the portion of cup enlargement that results from thinning of the prelaminar tissues due to physical compression and/or loss of retinal ganglion cell axons. We define laminar deformation or laminar cupping to be the portion of cup enlargement that results from permanent intraocular pressure (IOP)–induced deformation of the lamina cribrosa and peripapillary scleral connective tissues after damage and/or remodeling. We propose that the defining phenomenon of glaucomatous cupping is deformation and/or remodeling of the neural and connective tissues of the optic nerve head (ONH), which is governed by the distribution of IOP-related connective tissue stress and strain, regardless of the mechanism of insult or the level of IOP at which deformation and/or remodeling occurs. In other words, “glaucomatous cupping” is the term clinicians use to describe the clinical appearance and behavior the ONH assumes as its neural and connective tissues deform, remodel, or mechanically fail: 1) in a pattern and 2) by the several pathophysiologic processes governed by IOP-related connective tissue stress and strain. ONH biomechanics explains why a given ONH will demonstrate a certain form of “cupping” and at what level of IOP that might happen. Animal models are allowing us to tease apart the important components of cupping in IOP-related and non–IOP-related forms of optic neuropathy. A paradigm change in spectral domain optical coherence tomography ONH, retinal nerve fiber layer, and macular imaging should improve our ability to phenotype the ocular manifestations of many forms of damage to the visual system including glaucoma.

Optic Nerve Head Research Laboratory (CB), Devers Eye Institute, Optic Nerve Head Research Laboratory, Legacy Research Institute, Portland, Oregon.

Address correspondence to Claude Burgoyne, MD, Devers Eye Institute, Legacy Research Institute, 1225 NE 2nd Avenue (3rd Floor), Portland, OR 97232; E-mail:

C. Burgoyne is NIH funded to study the effects of aging in the monkey EG model using 3D histomorphometric techniques. He is also NIH funded to use SDOCT imaging to translate techniques developed in monkeys to human patient care. In this regard, he is a consultant to Heidelberg Engineering from which he receives unrestricted research support and occasional travel funds but no honorarium or personal income. He has received no travel support or honorarium to attend this meeting.

© 2015 by North American Neuro-Ophthalmology Society