All clinical cupping, regardless of etiology, is a manifestation of underlying prelaminar and laminar pathophysiologic components. (
A) Normal ONH. To understand the two pathophysiologic components of clinical cupping, start with (
B) a representative digital central horizontal section image from a postmortem 3-D reconstruction of this same eye (
white section line in
A): vitreous (
top), orbital optic nerve (
bottom), lamina cribrosa between the sclera and internal limiting membrane (ILM) (
green dots). (
C) The same section is delineated into principle surfaces and volumes (
black, ILM;
purple, prelaminar neural and vascular tissue;
cyan blue line, 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 (see
Fig. 4 ). (
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,
arrows) is primarily due to loss of prelaminar neural tissues without important laminar or ONH connective tissue involvement. Laminar or deep cupping (
H,
small white arrows) 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 whereas 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 damage followed by permanent (fixed) IOP-induced deformation.