Degenerative myopia (DM), also known as pathological myopia, is a severe, progressive form of nearsightedness. This condition involves structural changes to the eye that cannot be corrected with glasses or contact lenses alone. DM is a significant cause of irreversible vision loss and legal blindness worldwide, particularly among younger adults. The core issue is a progressive deformation of the eye’s shape, which compromises the health and function of light-sensitive tissues at the back of the eye.
Understanding High Myopia and Vision Risk
High myopia is defined as a refractive error of -6.00 diopters or greater, or an axial length—the measurement from the front to the back of the eyeball—of 26.0 millimeters or more. While many people with high myopia maintain stable vision, DM is characterized by ongoing, pathological changes to the eye’s inner structure. This distinction separates a refractive error from a progressive disease process.
The fundamental problem in DM is the excessive elongation of the eyeball, which stretches the delicate layers of the posterior eye wall. This stretching places mechanical strain on the retina, the choroid (the vascular layer beneath the retina), and the sclera (the outer white layer). These tissues become abnormally thinned and weakened as they are forced to cover an increasing surface area. This biomechanical stress initiates the degenerative cascade, creating an environment prone to severe complications.
This thinning often leads to an irregular outward bulging of the posterior sclera, known as a posterior staphyloma. The expansion and thinning of the eye wall compromises the blood supply and cellular integrity of the retina. These structural changes are the direct precursors to vision-threatening conditions that can lead to permanent loss of sight.
Specific Causes of Vision Impairment
The mechanical stress from elongation causes several pathologies, with myopic maculopathy being the most common cause of gradual central vision loss. This condition involves degenerative changes affecting the macula, the small central area of the retina responsible for sharp, detailed vision. These changes include progressive chorioretinal atrophy, where the layers of the retina and choroid waste away, leaving behind scarred, non-functional tissue.
A common finding in myopic maculopathy is the appearance of lacquer cracks, which are linear breaks in the Bruch’s membrane, the thin layer separating the retina and the choroid. These cracks represent areas of structural weakness that can lead to bleeding and scarring. They also serve as entry points for the most acute threat to central vision: choroidal neovascularization.
Choroidal neovascularization (CNV) occurs when abnormal, fragile blood vessels grow from the choroid through the damaged Bruch’s membrane into the subretinal space. These vessels leak fluid and blood, rapidly damaging the light-sensing cells of the macula, causing sudden vision distortion or a central blind spot. CNV affects approximately 5% to 11% of patients with pathological myopia and is the leading cause of rapid vision loss in individuals under 50 years old.
The stretching also affects the peripheral retina, leading to increased risk of retinal detachment. The thinned peripheral retina is susceptible to tears or holes, often preceded by lattice degeneration. If fluid separates the retina from its underlying support layers, a rhegmatogenous retinal detachment occurs. This is a medical emergency that can cause rapid loss of vision if not treated immediately.
Strategies for Monitoring and Treatment
Regular, comprehensive eye examinations are the most effective strategy for managing degenerative myopia and preventing vision loss. Frequent monitoring allows eye care professionals to identify subtle structural changes, such as new lacquer cracks or early signs of CNV, before they cause extensive damage. Specialized imaging techniques, including Optical Coherence Tomography (OCT), are used to visualize the retina’s cross-sectional layers and detect thinning or fluid accumulation.
The primary treatment for myopic CNV involves anti-Vascular Endothelial Growth Factor (anti-VEGF) medications. These drugs are delivered directly into the eye via an intravitreal injection to block the growth factor that stimulates the formation and leakage of abnormal blood vessels. Anti-VEGF therapy has stabilized the disease and often leads to sustained improvements in visual acuity.
When a retinal detachment occurs, surgical intervention is necessary to reattach the retina and preserve vision. Procedures such as scleral buckling or vitrectomy are performed to repair the tears and flatten the retina. For other complications, like myopic tractional maculopathy—where the vitreous gel pulls and splits the macula—surgery may be used to relieve the traction and prevent a macular hole.
While there are currently no treatments to reverse the eye’s axial elongation or prevent established degenerative changes, low-dose atropine drops are sometimes used in children to slow the progression of myopia. Patients with DM must remain vigilant about reporting any sudden changes in vision, such as new floaters, flashes of light, or central distortion, to their eye care provider without delay.