A3 Glaucoma: Optic Neuropathy due to Intraocular Pressure

Topic

The ciliary body—the same structure that controls lens accommodation in presbyopia—performs another function within the eye: it continuously produces aqueous humor, a clear fluid that fills the anterior chamber (the space between the cornea and the iris). The ciliary body never stops producing aqueous humor; consequently, the fluid must exit the eye at the same rate it is produced, or else it accumulates within the anterior chamber.

The aqueous humor accumulating in the anterior chamber exits the eye primarily through the trabecular meshwork—a porous structure located at the angle where the cornea and iris meet. This structure acts as both a filter and an outflow pathway for the fluid. The amount of aqueous humor the trabecular meshwork can drain at any given time depends on how freely the fluid can pass through it: an unobstructed meshwork allows the fluid to exit almost as quickly as the ciliary body produces it, whereas an obstructed or less permeable meshwork allows it to exit more slowly than it is being produced.

When the trabecular meshwork allows aqueous humor to exit more slowly than the ciliary body produces it, the undrained fluid accumulates in the anterior chamber. This accumulation raises intraocular pressure—the pressure the aqueous humor exerts against the inner walls of the eye. The greater the imbalance between aqueous humor production by the ciliary body and drainage by the trabecular meshwork, the higher the intraocular pressure rises; this elevated pressure is not confined to the anterior chamber but is transmitted throughout the entire eyeball, including the back of the eye. At the back of the eye, elevated intraocular pressure compresses the optic nerve right where its fibers exit the eyeball to travel toward the brain—a point that is structurally weaker than the rest of the eye wall. This sustained compression progressively damages the optic nerve fibers, starting with those that carry peripheral vision information; this progressive optic nerve damage caused by elevated intraocular pressure is known as glaucomatous optic neuropathy. The longer intraocular pressure remains elevated and uncorrected, the more optic nerve fibers are damaged and the more the person's visual field shrinks—starting at the edges and, if left untreated, progressing toward the center.

Since glaucoma stems from an imbalance between the production of aqueous humor by the ciliary body and its drainage through the trabecular meshwork, all treatments target one side of this imbalance. Pressure-lowering eye drops reduce intraocular pressure by acting on either side: beta-blockers reduce aqueous humor production by the ciliary body, while prostaglandins increase drainage via a pathway other than the trabecular meshwork. Laser treatment—specifically trabeculoplasty—acts directly on the trabecular meshwork to facilitate the outflow of aqueous humor. Similarly, surgery—whether trabeculectomy (creating a new drainage pathway) or minimally invasive glaucoma surgery (facilitating drainage with less trauma to the eye)—aims to restore the balance between aqueous humor production and drainage, thereby lowering intraocular pressure and relieving compression on the optic nerve.

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