Figure 7. A peripapillary scleral-lamina cribrosa dynamic underlies ONH biomechanics⁴⁸.

We propose that there are peripapillary scleral and lamina cribrosa contributions to ONH connective tissue behavior and that the manner in which the sclera canal and lamina cribrosa deform following a given level of IOP elevation in a given ONH will be determined by its level and duration and the structural stiffness of each tissue. Top Diagram. Normal lamina cribrosa (light blue), peripapillary sclera (slanted lines), Bruch's membrane (solid pink line), NCO (red points - in this schematic diagram, Bruch's membrane extends into the canal and is thus considered the neural canal opening (NCO)); Anterior scleral opening (blue points),NCO reference plane (small dotted red line), Border tissue of Elschnig (light green), choroid (black circles) and scleral portion of neural canal (orange). We define the structural stiffness of a tissue to be the combined function of both its connective tissue architecture (the quantity and distribution of load-bearing tissue) and material properties (the stiffness or compliance of the tissue) Bottom Diagram. Changes following acute IOP elevation in the monkey eye as depicted in this diagram can include: 1) posterior bowing of the ONH and circum-papillary sclera relative to the more peripheral peripapillary sclera (which manifest as an anterior deformation of the peripapillary sclera relative to the NCO reference plane); 2) axial thinning (orange lines are smaller in the high IOP eye) and radial expansion (angle theta has increased at high IOP) of the posterior scleral portion of the neural canal; 3) laminar thinning (solid blue at high IOP is less than low IOP); and 4) small anterior or posterior deformations of the anterior lamina cribrosa surface (black arrows and dotted blue lines). The effects of these deformations on astrocyte physiology, posterior ciliary artery blood flow and retinal ganglion cell axon axoplasmic transport and flow remain to be determined.