Age-related Macular Degeneration (or AMD), is the number one cause of visual loss among the elderly in the developed world. It involves the macula, an area with a diameter of a few millimeters, located in the center of the retina. This part of the retina is unique in several ways: it has no blood vessels of its own but is supplied by choroidal vessels situated underneath the retinal pigment epithelium.

The macula includes the highest concentration of photoreceptors, and is therefore responsible for fine vision, such as that needed for reading, writing, driving, face-recognition, or watching television. The remainder of the retina mostly provides information about movement in the visual field so that the eye or head can turn towards it and have that object’s image be focused on the macula.

In many persons as they age, the normal anatomy of the macula changes. The pathological process may involve genetical factors as well as various diseases and external factors such as hypertension, atherosclerosis, excessive sun exposure, or smoking.

Initially, small deposits develop in the retina, which are called drusen. Although these can block light from reaching the retina (a condition called negative scotoma), they are too small for the patient to recognize them – but they can signal the beginning of AMD.

AMD itself has two forms. The so-called “dry AMD” is a progressive, although slow, death of the photoreceptors and the retinal pigment epithelium, a process called atrophy. The resulting scar and loss of vision are irreversible.

The less common type of AMD (around 20% of all AMD cases) is called “wet AMD”. This is characterized by abnormal new blood vessels growing into the macula from the choroid, with exudation, bleeding, and the forming of a subretinal membrane. This process is driven by the secretion of a molecule called vascular endothelial growth factor or VEGF, which stimulates new vessels formation in the choroid. These abnormal new vessels have a porous wall, and fluid from inside the vessel pours into the otherwise dry retina. The fluid or bleeding causes an abrupt loss of central vision. The patient can also experience distortion of the image (for instance, crookedness of straight lines), and a decrease in color sensitivity. Eventually the photoreceptors are also destroyed.

It is important to understand that neither types of AMD causes total blindness or complete darkness; the central vision is affected but the visual field is maintained; the patient experiences a dark spot wherever he looks, so this dark spot moves as his eyeball moves. The patient maintains ambulatory vision and still perceives objects in the visual field, but it becomes impossible to read, write, drive, or recognize faces. Another common feature of AMD is that the visual problems cannot be corrected by glasses or contact lenses.


For dry AMD, no therapy is available today. Certain vitamin combinations have proven effective in slowing down the process, and it is crucial for the patient to take care of his systemic condition such as to normalize the blood pressure and blood cholesterol levels, and stop smoking.

For wet AMD, several treatment modalities have been developed.

• Thermal laser photocoagulation can destroy the new vessels and halt the progression. The unavoidable side effect is simultaneous destruction of the photoreceptors and the retinal pigment epithelium. Therefore this laser is indicated only in cases where the new vessels are outside the center of the macula.

• Surgical removal of the new vessels and the subretinal membrane, while anatomically successful, has largely been abandoned because the functional results were discouraging.

• Photodynamic therapy: A few minutes after injecting a photo sensitizer into the vein in the arm, a low-intensity laser is applied, which is able to spare the photoreceptors and the retinal pigment epithelium. Several sessions are often necessary. The treatment is painless, but for the next 48 hours the patient must avoid sun exposure to the skin and eyes.

• Surgical repositioning of the retina: called translocation, the retina is “moved” so that the still-functioning macula is placed on a healthy pigment epithelial bed. The operation is a difficult and complicated one, with a relatively low success rate.

• More recently, various molecules with anti-VEGF properties have been injected intraocularly. These drugs prevent VEGF from causing new vessel formation. They spare the photoreceptor and retinal pigment epithelial cells, and are able to improve, not just preserve, vision, but their effect is usually transitory. The injections often need to be repeated after 4 to 6 weeks. The patient must follow a rigorous follow-up schedule that includes retinal examination, angiography, and so-called OCT to detect recurrences early; in such cases, reinjections are needed.

The patient needs to know the following about the injection:
• Immediate see the ophthalmologist if vision gets worse.
• Do not to wear contact lenses for a week preceding the injection.
• On the day of the injection, avoid using a make-up.
• Do not wash the eye with soap for two days after the injection. Use the eyedrops that were prescribed, avoid contamination from infectious materials or persons. If the eye becomes red, painful, or there is unusual glare, call the ophthalmologist without delay.

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