Some of the greatest controversy surrounding NTG centers around the classification of the disease. Some investigators suggest that NTG is a disease process with its own separate risk factors and characteristics that should be distinguished from POAG. Others argue that, with increasing IOP, there is a continuum of increasing risk of developing POAG damage, and that NTG is simply at one end of that spectrum. Undoubtedly, POAG is a heterogeneous group of disorders, characterized by a final common pathway in which ganglion cells are lost in association with a characteristic excavation of the optic nerve head. Even in patients with NTG there are likely multiple disease processes represented. It is likely that in some patients with NTG glaucoma, IOP may play a role in the pathogenesis of the disease, as evidenced by the fact that even among eyes with statistically normal pressure, a further reduction in the IOP reduces the likelihood of progressive glaucomatous damage. What is left however, is a subset of subjects who progress despite a successful reduction in IOP. Do these patients simply require an even lower IOP for the safety of their ganglion cells and optic nerve? It seems that this may be true for some patients; however, for others, it is very likely that IOP does not play a dominant role in the disease process. For these patients, advances in the understanding of the molecular mechanisms of the disease will lead to novel diagnostic and treatment strategies that will be crucial in preventing progressive vision loss. It will be in this arena that some of the most exciting advances in the field of glaucoma will occur during the 21st century.
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