Pigment dispersion syndrome is associated with the development of glaucoma (known as pigmentary glaucoma). The lifetime risk of developing glaucoma in those affected by pigment dispersion syndrome has previously been recorded at around 50%. Pigment from the back of the iris is released into the front chamber of the eye and is deposited in various areas – onto the back of the cornea, and also onto the trabecular meshwork – the part of the eye that drains fluid out of the eye. Over many years, pigment dispersion within the eye can lead to elevated eye pressure, and this can lead to glaucoma. The reason why some people get pigment dispersion is that the shape of the iris tends to bow back towards the lens (that lies behind the iris). This concavity of the iris means that the pigment layer on the back of the iris can rub against the lens more readily. Performing an iridotomy (a tiny dot opening in the iris created by laser) is known to flatten the iris contour, presumably reducing pigment release. Laser is not performed in all cases. Another type of laser, laser trabeculoplasty is particularly effective in this condition.
Pigmentary glaucoma is a type of inherited open-angle glaucoma which develops more frequently in men than in women. It most often begins in the twenties and thirties, which makes it particularly dangerous to a lifetime of normal vision. Nearsighted patients are more typically afflicted. The anatomy of the eyes of these patients appears to play a key role in the development of this type of glaucoma. Let us examine why.
Myopic (nearsighted) eyes have a concave-shaped iris which creates an unusually wide angle. This causes the pigment layer of the eye to rub on the lens. This rubbing action causes the iris pigment to shed into the aqueous humor and onto neighboring structures, such as the trabecular meshwork. Pigment may plug the pores of the trabecular meshwork, causing it to clog, and thereby increasing the IOP.
Miotic therapy is the treatment of choice, but these drugs in drop form can cause disabling visual blurring in younger patients.
Fortunately, a slow-release form is available. Laser iridotomy is presently being investigated in the treatment of this disorder.
Examples of pigmentary glaucomas are shown in the images below.
To record changes in the pigmentation of the iris, the illumination beam must be directed coaxially through the pupil so that the retinal reflection appears in areas denuded of pigment granules. This transillumination photograph shows the sectoral defects associated with pigmentary glaucoma. Goniography uses diagnostic mirrored contact lenses to overcome corneal refraction and to permit visualization of the filtration angle. The pigment liberated from the iris in pigmentary glaucoma is shown in the angle, clogging the trabecular meshwork and impeding aqueous outflow.
Extensive fluctuations in intraocular pressure can occur in pigmentary glaucoma, often reaching very high levels. Spikes due to the sudden release of large amounts of pigment from the posterior iris can occur spontaneously, due to cycloplegia, or after vigorous physical activity.
Cycloplegia is paralysis of the ciliary muscle of the eye. This muscle plays an essential role in the focusing ability of the eye through a process called accommodation. Cycloplegia also compromises ciliary muscle tone on the trabecular meshwork, which negatively affects its filtering function and can result in elevated intraocular pressure.
Cycloplegia can be induced by drugs, trauma, or disease. For pigmentary glaucoma, the primary cause is disease, due to a condition called reverse pupillary block.
Normally, pressure between the anterior, posterior, and vitreous chambers of the eye is equalized. However, during pigment showers, outflow of aqueous humor through the trabecular meshwork temporarily can be impeded, raising pressure in the anterior chamber. The increased pressure within the anterior chamber forces the iris against the lens, causing the lens to block the open space of the pupil and thus maintaining the pressure disequilibrium between the chambers. The pressure difference causes a backward bowing of the iris. This concave configuration can cause a slight retraction of iris, so that it improperly inserts into the ciliary body, causing cycloplegia.
Although pigment showers caused by vigorous physical activity do not occur in every patient, release of pigment from the iris, regardless of the mechanism, is thought to obstruct aqueous humor outflow by overwhelming the drainage angle of the anterior chamber. A majority of the liberated pigment appears to pass eventually through the trabecular meshwork and into Schlemm’s canal, as elevations in intraocular pressure tend to be transient and last just a few hours. Once in Schlemm’s canal, the pigment granules are absorbed into pores within and between cells.
Damage to the optic nerve varies with the extent and duration of elevated intraocular pressure. Beyond this, pigmentary glaucoma displays typical signs and symptoms observed in primary open-angle glaucoma.
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