The morphological difference between glaucoma and other optic neuropathies.

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.