Myopia, commonly known as nearsightedness, is a refractive error where the eye focuses light in front of the retina, making distant objects appear blurry. Degenerative myopia, also called pathological myopia, is a severe, progressive form of this condition. It is characterized by destructive structural changes at the back of the eye that threaten vision, representing a disease process rather than just a strong prescription.
Distinguishing Degenerative Myopia from High Myopia
Myopia is generally categorized based on the spherical equivalent refractive error, measured in diopters (D). Low myopia is typically defined as a refractive error between -0.50 D and less than -6.00 D. High myopia refers to a more severe refractive error of -6.00 D or worse.
The distinction between high myopia and degenerative myopia is based on structure, not just the power of the glasses needed. Degenerative myopia is defined by the presence of pathological changes in the posterior segment of the eye, such as myopic maculopathy or a posterior staphyloma. These structural changes can lead to vision loss, regardless of whether the refractive error meets the -6.00 D threshold. While most cases occur in eyes with high myopia, the terms are not interchangeable, as not every highly myopic eye develops these pathological changes.
A posterior staphyloma is the most defining structural feature of the degenerative form, characterized by an outward bulging and thinning of the posterior wall of the eye. This localized deformation stretches the overlying retina and choroid, setting the stage for various complications. The presence of this bulging or myopic maculopathy officially classifies the condition as pathological.
Genetic and Structural Basis of Progression
The primary mechanism driving degenerative myopia is excessive axial elongation, meaning the eyeball grows too long from front to back. A normal adult eye typically measures about 24 millimeters in axial length, but in high myopia, this length often exceeds 26 to 26.5 millimeters. This abnormal growth stretches the entire posterior structure of the eye, including the sclera, choroid, and retina, thinning these layers like rubber pulled taut.
Genetics play a significant role in determining susceptibility to this excessive growth, with studies identifying over 200 genetic loci associated with myopia. These genes are implicated in processes like the regulation of eye growth and the formation of collagen, which provides structural support to the eye wall. This strong heritable component explains why the condition often runs in families, predisposing individuals to the rapid progression and structural changes. The biomechanical stress from elongation directly causes the pathological thinning and damage to the retina and choroid.
Serious Associated Complications
The stretching and thinning of the posterior eye tissues create a high risk for several vision-threatening complications. The most common of these is Myopic Macular Degeneration (MMD), also referred to as myopic maculopathy. MMD involves progressive damage to the macula, the central part of the retina responsible for sharp, detailed central vision.
This maculopathy can manifest as lacquer cracks, which are fine linear breaks in the Bruch’s membrane layer beneath the retina, or as myopic foveoschisis, which is the splitting of the retinal layers due to traction. Another manifestation is Choroidal Neovascularization (CNV), where fragile, abnormal new blood vessels grow beneath the retina in an attempt to repair the damaged tissues. These new vessels often leak fluid and bleed, causing rapid and severe loss of central vision.
The thinning and weakening of the retina significantly increase the risk of Retinal Detachment (RD). Traction and tears in the stretched retina can cause it to pull away from its underlying support layers, requiring immediate surgical intervention to prevent permanent blindness. The elongated shape of the eye is also associated with an increased risk of developing Glaucoma. This condition involves damage to the optic nerve, often linked to increased pressure inside the eye, which can lead to progressive peripheral vision loss.
Monitoring and Treatment Approaches
Managing degenerative myopia focuses on the early detection of complications and intervention to prevent further vision loss. Regular, comprehensive eye examinations are necessary, often including imaging like Optical Coherence Tomography (OCT). OCT scans provide high-resolution cross-sectional images of the retina, allowing specialists to monitor for layer splitting, fluid buildup, and the development of new blood vessels.
Treatment is primarily aimed at addressing the complications once they arise. For Choroidal Neovascularization, treatment involves anti-VEGF (anti-vascular endothelial growth factor) injections. These medications are injected into the eye to block the chemical signal that causes abnormal blood vessels to grow and leak, helping to stabilize or improve vision. Retinal detachment and severe foveoschisis often require surgical procedures, such as a vitrectomy, to reattach the retina and relieve mechanical traction.
While glasses or contact lenses can correct the refractive error, they do not treat the underlying pathological changes. For individuals who experience permanent vision loss from the complications, low-vision aids and rehabilitation services become an important part of management to help them maximize their remaining sight. The goal of ongoing care is to preserve as much functional vision as possible by diligently monitoring and treating any new pathological signs.