ABSTRACT
Ophthalmic hypertension and primary open-angle glaucoma are stages of the same process aimed at creating comfortable conditions for accommodation apparatus performance in anatomically poor eyes. Ophthalmic hypertension is a compensatory reaction to decreased ciliary muscle performance. It is induced by increased blood flow to the anterior eye segment, which improves metabolism in the ciliary body and enhances its performance capacity. Aqueous humor hyperproduction elevates pressure, without causing the eye to stretch due to the compensatory consolidation of a scleral capsule. The above processes fail to damage visual functions in 2/3 patients with ophthalmic hypertension. There is depletion of the body's compensatory capacities and ophthalmic hypertension progresses to glaucoma in a third of patients (this seems to be genetically determined). At the stage of glaucoma, a reverse compensatory reaction (eye ischemization and scleral sprain) is engaged to make accommodation apparatus performance easier. However, a third of patients gets into the vicious circle and loses their vision.
