Glaucoma is a term applied to a group of eye diseases that cause a characteristic and recognizable deterioration of the optic nerve. The optic nerve carries visual information from the eye to the brain, much like the cable from a computer screen to the computer. In the brain, it is assembled into a visual image that we recognize as sight.
Glaucoma Definition
The simplest definition of glaucoma is that condition of the eye where the intraocular pressure is elevated beyond the limit that will permit normal function of the optic nerve. However, there are two parts to the definition. First, it implies the presence of abnormal intraocular pressure, generally above 21 mm Hg, which is somehow due to an abnormality in aqueous drainage from the eye, or impediment to aqueous flow from the posterior to the anterior chamber of the eye; second is the suggestion that the intraocular pressure somehow embarrasses the nerve fibers ganglion cells, the final neural pathway from the eye to the brain. The fact that this definition is simplistic is easily demonstrated be the patient with the so-called "normal" intraocular pressure, generally below 21 mm Hg, who has typical glaucomatous cupping of the optic nerve head and characteristic visual field defects. Then there is the patient with the marked elevation in ocular pressure, usually from an inflammatory condition, who sustains no optic nerve alternations even after a protracted period of time. Thus, glaucoma defies a simple explanation.
When the optic nerve is damaged or injured, the transmission of visual information and, hence, the visual image is impaired. Fortunately, ophthalmologists can usually detect glaucomatous optic nerve damage before there is noticeable visual loss by examining the back of the eye. Sometimes, damage to the nerve can be observed before there is a change in vision by specialized tests of vision.
Causes of Glaucoma – Optic Nerve and Pressure
In many cases, glaucoma optic nerve damage occurs from high eye pressure. Nerve damage can usually be stopped or slowed by lowering the eye pressure. Most glaucoma treatment, with medicines, laser, or conventional surgery, is designed only to lower the eye pressure. Some eyes with glaucoma optic nerve damage continue to deteriorate despite having the lowest possible eye pressures. It is not known why this happens. Intensive research around the world is now directed at understanding the cause of the damage in these patients and to develop new treatments to preserve the optic nerve.
Many different eye disorders cause high eye pressure. After measuring the eye pressure, your ophthalmologist attempts to determine the cause of the elevation. Nearly always, some form of "clogging" or blockage of the drainage of internal fluid within the eye (aqueous humor) causes increased eye pressure. Since the eye continually produces this fluid, obstruction of the drainage causes the eye pressure to increase. Almost any eye disorder associated with aging, inflammation, bleeding, injury, tumor or even birth defects can raise the eye pressure. However, in most cases of glaucoma, the eye has no specific abnormality and is said to have primary open-angle glaucoma. In other cases, the eye may be unusually small or exhibit other minor shape abnormalities that cause closed-angle glaucoma. In closed-angle glaucoma, the drainage system is totally blocked instead of just being clogged.
At least fifty different mechanisms have been described that can raise the eye pressure, but all produce similar damage of the optic nerve. All methods of glaucoma treatment are designed to lower the eye pressure to a level that will prevent further optic nerve damage.
"How's My Optic Nerve, Doctor?"
Ongoing assessment of glaucoma depends upon regular examination of the optic nerve and visual field in addition to the eye pressure. The well informed glaucoma patient asks not "What is my eye pressure, doctor?," but rather, "How is my optic nerve?"
Comprehensive Definitions of Glaucoma
Acute Angle-Closure Glaucoma
Acute Angle-Closure Sequelae
Angle Closure Secondary
Chronic Angle-Closure Glaucoma
Normal Angle Vessels
Plateau Iris Syndrome
Primary Open-Angle Glaucoma
Normal Anterior Chamber Angle Measurement
Optic Nerve Cupping in Glaucoma
Acute Angle-Closure Glaucoma
Oblique flashlight illumination showing shallow anterior chamber, corneal edema and mid-dilated pupil. Gonioscopic appearance shows closed angle without any visible angle structures. Note how the corneal beam tapers towards the Schwalbe's line.
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Acute Angle-Closure Sequelae
There are numerous sequellae of an acute angle-closure attack. Vision is often affected and visual recovery is variable. Following an attack the cornea frequently develops folds in Descemet’s membrane; recovery is usually complete, although some degree of endothelial cell loss may occur. Occasionally, chronic corneal edema develops despite normalized intraocular pressure. This most often occurs in patients with pre-existing Fuch’s dystrophy, or long-standing angle-closure prior to treatment.
Frontal view showing shallow anterior chamber, diffuse iris stromal atrophy, spiraling of the iris stroma inferiorly, and glaukomflecken of the lens. Gonioscopy shows permanent synechial closure.
Angle-Closure Secondary
Primary cysts of the iris and ciliary body are uncommon, and only rarely cause glaucoma. Recently, however, Vela and colleagues reported three families in whom angle- closure glaucoma occurred in 4 of 11 patients with such cysts. It was suggested that in some instances of such cysts there may be autosomal dominant inheritance. There are no known systemically related disorders.
In instances where the intraocular pressure suddenly rises, pilocarpine can normalize the pressure. Peripheral and sector iridectomies have been relatively unsuccessful in managing these patients. Pigmented iris cysts can be treated by puncturing their walls with argon laser photocoagulative surgery. However, the cysts may redevelop and again close the angle. The nonpigmented ciliary body cysts do not respond to argon laser treatment. In time, the affected patients may have to undergo standard filtering surgery to control their secondary synechial angle closure glaucoma.
Patients with angle-closure glaucoma secondary to iris and ciliary body cysts should be carefully followed and their family members examined and appropriately counseled.
Multiple pigment cysts of the iris can be seen through the dilated pupil. The angle is irregularly narrowed and a broad peripheral anterior synechiae has formed.
Chronic Angle-Closure Glaucoma
Primary angle-closure glaucoma caused by a pupillary block mechanism can be divided into either acute or sub-acute angle-closure or chronic angle-closure. The initiating event is a functional block between the anterior lens surface and the posterior pupillary portion of the iris. This results in trapping of aqueous in the posterior chamber thus pushing the peripheral iris forward and closing of the angle. Outflow resistance increases, intraocular pressure rises, and with time permanent synechial closure ensues.
Oblique flashlight illumination showing shallow anterior chamber, corneal edema and mid-dilated pupil. Gonioscopic appearance (above) shows closed angle without any visible angle structures. Note how the corneal beam tapers towards the Schwalbe's line.
Normal Angle Vessels
Normal Angle Vessels / Composite drawing of normal vessels seen in normal eyes
- Radial ciliary body or trabecular vessel
- Radial iris vessel
- Circular ciliary band vessel
Plateau Iris Syndrome
The plateau iris configuration refers to an anterior chamber of normal depth axially with a flat iris plane on direct examination but a narrow angle on gonioscopic examination. The plateau iris syndrome refers to the clinical picture either of spontaneous or mydriatic-induced angle-closure despite a patent iridectomy. In the majority of cases of angle-closure glaucoma associated with the plateau iris configuration, iridectomy is curative. The widening of the angle is not as dramatic and may not only be limited to the iris periphery. If iridectomy fails, the plateau iris syndrome should be considered. The plateau iris syndrome must not be confused with other conditions such as imperforate iridectomy associated with angle closure, elevated intraocular pressure from residual peripheral anterior synechiae, angle closure due to multiple cysts of the ciliary body, and mydriatic-induced intraocular pressure rise without angle closure. Once the diagnosis of plateau iris syndrome is made, the treatment is by continuous use of miotics. If miotics cannot be tolerated, laser iridoplasty(gonioplasty) has been reported to be curative.
Axial portion of the anterior chamber is of normal depth and an iridectomy is present at at 11 o'clock. The plane of the iris is vertical, and the iris root undergoes a knee-shaped bend (insert lower right) in the extreme periphery, causing sudden narrowing of the angle in the presence of a patent iridectomy. Insert upper right shows a closed angle in spite of a deep central anterior chamber.
Primary Open-Angle Glaucoma
The cause of POAG is unknown, but it has been suggested that there are multifactorial heritable factors; in many cases there is a strong family history of the disorder. To date, no specific histopathological abnormality has been noted.
The anterior segment including the angle appears to be within normal limits.
Normal Anterior Chamber Angle Measurement
Composite drawing of the normal angle seen in normal eyes. Various widths of the normal angle seen in consecutive inserts. Note that the corneal optical wedge narrows as it approaches Schwalbe's line and seems to end there in the situation of a narrow angle.
a) Schwalbe's line b) Trabecular meshwork c) Scleral spur d) Ciliary body band e) Peripheral
Optic Nerve Cupping in Glaucoma
Damage to the nerve fibers of retinal ganglion cells is the most important sequellae of glaucomatous disease and is manifest clinically by alterations in the appearance of the optic disc. the pathogenic mechanism(s) by which an abnormality of intraocular pressure eventually results in retinal nerve fiber degeneration is a matter of intense debate. Histopathologic examination of the damaged optic nerve head reveals not only axonal degeneration of retinal ganglion cells but also loss of astroglial support tissue, reduction in disc vascularity, and collapse of the lamina cribrosa. Primary vascular, mechanical, and glial theories have all been suggested. Regardless of its etiology, there is a rather typical sequence of change that occurs to the optic disc in uncontrolled glaucoma.
Normal optic nerve head with small central physiologic cup, C/D ratio about 0.2
Concentric enlargement of the central cup, C/D ratio about 0.5
Irregular enlargement of the cup, especially inferiorly due to loss of inferior neural rim tissue
Marked glaucoma cupping with high degree of central atrophy, C/D ratio 0.7 to 0.8
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