The pathogenesis of glaucoma is mainly: the circulatory balance of fluid in the eye is disrupted for various reasons, resulting in an increase in intraocular pressure that exceeds the level tolerated by the optic nerve, thus causing optic nerve damage and visual field defects. It is because the volume of the eye is relatively fixed, so changes in the crystalline lens, vitreous humor, intraocular blood and atrial fluid, which constitute the contents of the eye, are necessarily accompanied by changes in intraocular pressure. Traditionally, the first three are not considered to change much. Only the dynamic balance of the atrial circulation most directly affects the stability of intraocular pressure. An impairment at any point along the way of the atrial circulation will affect the balance between atrial aqueous production and discharge, manifesting itself as a change in high or low IOP. There are three pathophysiological processes involved in the elevation of IOP in glaucoma; an increase in the rate of atrial aqueous production by the ciliary process, an increase in resistance to atrial aqueous flow out through the trabecular meshwork pathway, and an increase in venous pressure in the surface sclera. The vast majority of glaucoma in clinical practice is due to increased resistance to atrial outflow. There are a number of clinically effective measures in place. The main principle is to improve atrial aqueous circulation, regain equilibrium, and reduce pathologically elevated intraocular pressure. This will stop and prevent damage to the retinal optic nerve and protect visual function. In summary, the cause of glaucoma is elevated intraocular pressure, which, in turn, is mainly caused by obstruction of atrial aqueous drainage.