Recent pathogenic concepts of primary open angle glaucoma and soft glaucoma (POAG).

Loss of mainly field in POAG is due to Schnabel's cavernous atrophy of the axons at their scleral passage, built up by aligned stacks of glial collagen (IV and I) tissue plates, which contain capillaries. Organisation, size and structural surroundings encircle isolated or grouped axons not evenly distributed. The stereotype pattern of fieldloss linked to a characteristic optic nerve lesion suggests POAG be considered a N.O. disease as raised IOP may be only one of the risk factors. Are cavernous atrophy (loss of field) and the trabecular spaces narrowing (rise of IOP) both the result of the same pathogenic mechanism acting on the collagen fiber (IV and I) of the scleral coat, resp. lamina cribrosa (posterior segment) and trabecular meshwork (anterior segment)? If so, IOP-rise only worsens the condition as will do a hemodynamic energy crisis at the level of the axons. Interactive dominance at any of both levels may explain unexpected discrepancies between IOP and fieldloss. Considering "to treat or not to treat" accurate field loss predictability testing, urgent research topic, are discussed.