“…The classic physiopathology theory of glaucoma poses that an increase in intraocular pressure (IOP) would lead to compression of the axons at the lamina cribrosa (LC) with consequent ischemia and axoplasmic flow blockage, and hence the death of RGC [ 2 ]. However, although high IOP is recognized as the most important risk factor for glaucoma [ 3 ], this is not the only mechanical load experienced by the optic nerve, as it is also influenced by cerebrospinal fluid pressure [ 4 , 5 ], IOP fluctuations [ 6 ], vascular pulsatility [ 7 ], and eye movements [ [8] , [9] , [10] , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] ], among other factors.…”