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After being produced by the ciliary body, the aqueous humor enters the posterior chamber (the space between the iris and the zonules) before passing through the pupil to enter the anterior chamber (between the iris and the cornea).

From that site it drains into veins by way of the trabecular meshwork and Schlemm’s canal.

A delicate balance between the production and drainage of the aqueous humor maintains transocular pressure within its physiological range (10-20 mm Hg).

 In certain pathologic states aqueous humor accumulates within the eye, and the intraocular pressure, which is measured by determining the force required to indent or flatten the cornea, becomes elevated , producing temporary or permanent impairment of vision and damage to the optic nerve.

When this occurs, usually when the intraocular pressure is above 20 mm Hg, the term glaucoma is applied.

Vision becomes impaired because of degenerative changes in the retina and optic nerve head (a result of ocular hypertension and resultant ischemia), and because of corneal edema and opacification.

Effects of Elevated Intraocular Pressure:

Individuals vary in their ability to tolerate an elevated intraocular pressure. Some do not develop a visual field loss or optic atrophy after having an intraocular pressure of three standard deviations above the mean (24 mm Hg) for many years.

Prolonged ocular hypertension has several effects on the eye:

1.  In adults it leads to a characteristic cupped excavation of the optic disc (glaumatous cupping), accompanied by a nasal displacement of the retinal blood vessels. In infants cupping of the optic disc tend to be less prominent.

2.  The cornea or sclera bulges at weak points, such as sites of scars in the outer coat of the eye.

3. Optic atrophy, with a loss of axons, gliosis, and thickening of the pial septa, follows the retinal degeneration and damage to the nerve fibers at the optic disc.

4. The ganglion cell layer of the retina degenerates, thereby impairing vision. The outer retina, which derives its nutrition from the underlying choroids, remains intact.

5. When the intraocular pressure becomes elevated before the age of 3 years, the pliable eye sometimes enlarges extensively and may resemble an ox eye (buphthalmos). After the first few years of life, a rigid sclera prevents glaumatous eyes from enlarging under the elevated pressure.

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New perspectives in aqueous humor secretion and in glaucoma: The ciliary body as a multifunctional neuroendocrine gland.Prog Retin Eye Res. 2007 Jan 17;

The discovery in the human ocular ciliary body of glaucoma-associated genes (i.e., MYOC, CYP1B1), neuroendocrine-processing enzymes, neuroendocrine peptides, steroid-converting enzymes, glutamate transporters, glutamate-metabolizing enzymes, and anti-angiogenic factors requires a reevaluation of its function on aqueous humor secretion, intraocular pressure and its role in glaucoma. The ciliary body should be considered as a multifunctional and interactive tissue. The intrinsic hypotensive and/or hypertensive biological activities of many of the endocrine peptides released by the ciliary epithelium are best explained within the context of a neuroendocrine system, linking the inflow and the outflow of aqueous humor. This interpretation is consistent with physiological and genetic studies indicating that changes altering the inflow affects intraocular pressure. In the proposed endocrine system, regulatory peptides secreted by the ciliary epithelium may subserve multiple functions in the following: inflow and outflow pathways of aqueous humor, ciliary blood flow, the immune privilege status of the anterior segment and the diurnal circadian rhythms of aqueous humor secretion and intraocular pressure. These previously unsuspected and challenging functions of the ciliary epithelium should be considered when assessing the multifactorial events which lead to the pathophysiology of glaucoma affecting the outflow pathways of aqueous humor. This review highlights published, and ongoing studies on authors' labs supporting neuroendocrine, steroidogenic and glutamatergic features of the ciliary epithelium and the endocrine communication between the inflow and outflow pathways of aqueous humor. We also discuss how glaucoma-associated genes expressed in the ciliary body and their mutant proteins could influence intraocular pressure, contributing to the development of glaucoma.

           

Influence of prostaglandins on aqueous humour dynamics and intraocular pressure.Klin Monatsbl Augenheilkd. 2005 Oct;222(10):802-6.

In the glaucoma disease the disturbed trabecular outflow results not only in an increase in the intraocular pressure (IOP) level, but also in an increase in the intraocular pressure fluctuations in the majority of patients. This induces a biomechanical stress that may damage the optic nerve head over time and may result in the typical glaucomatous excavation. Prostaglandin analogues show positive effects on both risk factors. They enhance the uveoscleral outflow of the aqueous humour, improve the trabecular outflow facility and probably the regulatory capacity of the trabecular meshwork itself. This dual mechanism might explain the strong IOP-lowering efficacy of the prostaglandins and their additional property to reduce IOP fluctuations leading to a general improvement of the aqueous humour dynamics. Therefore, it makes sense pharmacologically to combine prostaglandins with those medications that also reduce aqueous humour production.

 April 2007

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