The eye requires precise internal pressure to maintain its shape and function. This pressure is regulated by a delicate balance between the production and drainage of a clear fluid called aqueous humor. A small, circular structure manages the majority of this drainage process. Understanding the role of Schlemm’s Canal is fundamental to grasping how the eye maintains its stability and how diseases that disrupt this system can lead to vision loss.
Defining Schlemm’s Canal and Aqueous Humor Flow
Schlemm’s Canal is a specialized, ring-shaped vessel located at the perimeter of the iris, near the junction where the cornea meets the sclera. This canal acts as the final collection point for the eye’s drainage system. It is an endothelium-lined tube that ensures the controlled exit of fluid from the eye’s anterior chamber.
The aqueous humor is a transparent fluid produced continuously by the ciliary body behind the iris. This fluid provides nutrients and oxygen to tissues lacking a direct blood supply, such as the cornea and the lens. After production, the fluid flows through the pupil into the anterior chamber, where it collects before draining out.
The primary route for the aqueous humor’s exit, the conventional outflow pathway, is through the trabecular meshwork. This meshwork is a spongy, sieve-like tissue situated directly over the inner wall of Schlemm’s Canal. The fluid filters through the meshwork’s spaces and enters the canal, which then connects to a network of collector channels and episcleral veins.
Approximately 80% to 90% of the aqueous humor drains through this mechanism. By controlling the rate at which fluid leaves the eye, Schlemm’s Canal ensures a steady internal pressure (IOP). A healthy, open canal is necessary to maintain fluid homeostasis and prevent internal pressure from rising.
Schlemm’s Canal Dysfunction and Elevated Eye Pressure
When the outflow pathway involving Schlemm’s Canal is dysfunctional, resistance to fluid movement increases, causing intraocular pressure (IOP) to rise. This sustained high pressure is the primary risk factor for Primary Open-Angle Glaucoma (POAG), a progressive disease that damages the optic nerve. The damage results from the mechanical and vascular stress caused by the chronically elevated IOP.
In most cases of POAG, the angle where the iris meets the cornea remains physically open, meaning the problem is not a simple structural blockage. Resistance is localized within the filtration apparatus, specifically in the juxtacanalicular tissue immediately adjacent to the canal’s inner wall. Pathological changes in the cells and matrix in this region hinder the smooth filtration of aqueous humor.
One specific change is an increase in tissue stiffness and a reduction in the porosity of the inner wall of Schlemm’s Canal. Stiffer cells impede the formation of the large vacuoles necessary for fluid transfer. This stiffening acts like a less flexible filter, increasing the resistance the aqueous humor encounters before entering the canal.
Furthermore, the canal’s structure can be compromised in glaucomatous eyes, often exhibiting a reduced cross-sectional area. This narrowing can be exacerbated by elevated pressure, causing the canal to partially collapse and restrict outflow. The blockage is compounded by the herniation of trabecular meshwork tissue, which can obstruct the orifices of the collector channels. This cycle of increased resistance and structural compromise leads to the progressive nature of the disease.
Therapeutic Strategies Targeting Drainage
Treating glaucoma relies on lowering intraocular pressure (IOP), and many modern therapies are designed to improve or bypass the dysfunctional drainage system. Medical treatments, typically eye drops, work by either decreasing the production of aqueous humor or increasing its outflow. Prostaglandin analogs primarily enhance the unconventional drainage route through the uveoscleral pathway, while other drops target the conventional pathway.
Medications like Rho Kinase (ROCK) inhibitors specifically target cells within the trabecular meshwork and Schlemm’s Canal. These drugs promote the relaxation and loosening of the meshwork’s tissue and the canal’s endothelial cells. By reducing the stiffness and contractility of these cells, ROCK inhibitors decrease resistance to flow, enhancing natural drainage into the canal.
Surgical interventions, particularly Minimally Invasive Glaucoma Surgery (MIGS), are frequently used to address the canal’s pathology directly. These procedures often create a bypass or restore the canal’s function:
- Micro-stent insertion, such as the iStent, creates a microscopic bypass channel allowing aqueous humor to flow directly into Schlemm’s Canal, circumventing the primary site of resistance.
- Goniotomy and trabeculotomy use specialized instruments to remove a portion of the trabecular meshwork. This action unroofs Schlemm’s Canal, directly exposing it to the anterior chamber and significantly lowering the outflow resistance.
- Canaloplasty involves threading a microcatheter around the canal’s circumference and injecting a viscoelastic gel to dilate and widen the channel.
These drainage-focused strategies aim to restore the eye’s natural fluid balance, managing the pressure that causes optic nerve damage.