All clinical cupping, regardless of etiology, is a manifestation of underlying prelaminar and laminar pathophysiologic components. (
A) Normal optic nerve head (ONH). To understand the two pathophysiologic components of clinical cupping, start with (
B), a representative digital central horizontal section image from a postmortem 3D reconstruction of this same eye (
white section line in [
A]), vitreous top, orbital optic nerve bottom, and lamina cribrosa between the sclera and internal limiting membrane (ILM) delineated with
green dots. (
C) The same section is delineated into principal surfaces and volumes (
black, ILM;
purple, prelaminar neural and vascular tissue;
cyan-blue line, Bruch's membrane opening [BMO] zero reference plane cut in section;
green outline, post-BMO total prelaminar area or a measure of the space below BMO and the anterior laminar surface). (
D) Regardless of the etiology, clinical cupping can be shallow (
E) or deep (
F) (these clinical photographs are representative and are not of the eye in [
A]). A prelaminar or shallow form of cupping (
G,
black arrows) is primarily due to loss (thinning) of prelaminar neural tissues without important laminar or ONH connective tissue involvement. Laminar or deep cupping (
H,
small white arrows depict expansion of the
green-shaded space) follows ONH connective tissue damage and deformation that manifests as expansion of the total area beneath BMO but above the lamina. Notice in (
H) that while a laminar component of cupping predominates (
white arrows), there is a prelaminar component as well (
black arrows). Although prelaminar thinning is a manifestation of neural tissue damage alone, we propose that laminar deformation can occur only in the setting of ONH connective tissue deformation and remodeling. Reprinted with permission from Yang H, Downs JC, Bellezza A, et al. 3-D histomorphometry of the normal and early glaucomatous monkey optic nerve head: prelaminar neural tissues and cupping.
Invest Ophthalmol Vis Sci. 2007;48:5068–5084.
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