Open angle glaucoma is characterized by optic atrophy, field loss corresponding to a nerve fiber bundle distribution, increased outflow resistance, and elevated intraocular pressure. Clinical signs or manifestations of different pathogenetic processes appear quite similar because tissues have only a limited number of visible reactions to different insults. The final pathway for damage is common, but the initiating or primary mechanisms for damage may vary. It would not be difficult to imagine that glaucoma represents a syndrome, a final collection of similar signs produced by different pathogenetic mechanisms. The disease would then comprise subgroups, each with signs and sequences of signs that vary in both space and time.
For example, there are individuals whose glaucomatous field loss progresses at both an early and a late phase of disease in spite of what is ordinarily considered adequate pressure control. In his time, Gifford1 was one among several ophthalmologists who, along with
Sears ML. Clinical and Scientific Basis for the Management of Open Angle Glaucoma. Arch Ophthalmol. 1986;104(2):191–195. doi:10.1001/archopht.1986.01050140045017
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