Neovascular Age-related Macular Degeneration (nAMD) is a progressive eye condition affecting the macula, the central part of the retina responsible for sharp, detailed vision. This disease represents a late, advanced stage of age-related macular degeneration (AMD) and is a leading cause of severe and irreversible vision loss globally in people over the age of 60.
Defining NAMD Disease
Neovascular Age-related Macular Degeneration is characterized by choroidal neovascularization (CNV), the abnormal growth of new, fragile blood vessels beneath the macula. This growth is driven primarily by the overexpression of vascular endothelial growth factor (VEGF). These abnormal blood vessels are weak and prone to leakage, releasing fluid and blood into the retinal layers. This leakage damages light-sensing cells and causes scarring of the macula, which is why the condition is often called “wet” AMD, in contrast to the “dry” form involving drusen deposits.
The development of nAMD stems from a complex interplay of genetic and environmental factors. Genetic predisposition plays a significant role, with a strong family history of AMD increasing an individual’s risk. Environmental factors, particularly smoking, dramatically increase the likelihood of developing nAMD, making smokers two to five times more susceptible.
While the disease typically manifests in individuals in their sixties and seventies, women and Caucasian populations exhibit a higher risk profile. The presence of non-neovascular (dry) AMD often precedes the development of nAMD. Approximately 15% of dry AMD cases progress to the wet form, which accounts for the majority of AMD-related severe vision loss.
Recognizing the Signs
The clinical presentation of nAMD involves symptoms related to the rapid deterioration of central vision. One common early indicator is metamorphopsia, where straight lines appear wavy, bent, or distorted. Patients may notice this when looking at door frames, utility poles, or the lines on an Amsler grid. This visual distortion is caused by fluid accumulation from leaky vessels separating the retinal pigment epithelium from the outer retina.
As the condition progresses, individuals often experience a gradual or sudden blurring of their central vision, making detailed tasks difficult. This can significantly impair the ability to read, drive, or recognize faces. A scotoma, or a blind spot in the center of the field of vision, is another advanced sign that develops as the macula sustains damage.
Difficulty distinguishing between colors or noticing a general dimness in vision can also occur. Since nAMD can initially affect only one eye, patients may not immediately recognize the symptoms, as the unaffected eye compensates for the loss. Individuals with known dry AMD should monitor their vision closely, as the change to the neovascular form can sometimes be rapid.
Diagnostic Procedures
Confirming a diagnosis of nAMD requires specialized examinations and imaging tests performed by an eye care professional. The process often begins with a measurement of visual acuity to quantify the degree of central vision loss. The Amsler grid test, an at-home screening tool, allows the patient to monitor for distortion or missing areas in a grid pattern, providing preliminary evidence of macular issues.
A dilated retinal examination allows the clinician to visualize the back of the eye for signs of CNV, hemorrhage, or fluid leakage. Optical Coherence Tomography (OCT) is a primary diagnostic tool, using light waves to capture high-resolution, cross-sectional images of the retina. OCT scans precisely detect and measure fluid within or beneath the retina, which is a definitive sign of active nAMD.
Fluorescein Angiography involves injecting a fluorescent dye into an arm vein. As the dye circulates through the eye’s blood vessels, a specialized camera captures images, highlighting any areas of leakage from the abnormal neovascular membranes. This test helps map the exact location and extent of the leaky vessels.
Therapeutic Approaches
The current standard of care for nAMD focuses on pharmacological interventions aimed at stopping the growth and leakage of the abnormal blood vessels. These treatments, known as anti-VEGF agents, are administered through intravitreal injections directly into the eye. Anti-VEGF medications work by binding to and neutralizing the vascular endothelial growth factor (VEGF) protein.
Common anti-VEGF medications include:
- Ranibizumab
- Aflibercept
- Brolucizumab
- Faricimab
Regular injections of these drugs, often monthly or bi-monthly, can significantly improve visual acuity and prevent further vision loss in a majority of patients. While these treatments are highly effective, the need for frequent injections is a primary challenge for long-term patient compliance. Extended-interval dosing regimens are continually being developed to reduce the burden of treatment.
Newer drugs target both the VEGF and angiopoietin pathways, allowing for treatment intervals of up to 16 or 24 weeks for some patients. Gene therapy is an emerging approach that aims to provide a long-term, potentially one-time treatment by instructing the eye’s cells to continuously produce their own anti-VEGF protein. Long-term management of nAMD also includes supportive care, such as low-vision aids and rehabilitation services, to help individuals maximize their remaining vision.