Myopia, commonly known as nearsightedness, is a refractive error where distant objects appear blurred because the eye focuses light in front of the retina. Pathological myopia (PM), however, is a severe, progressive form of the condition that transcends a simple refractive issue to become a degenerative eye disease. PM is characterized by chronic, irreversible structural changes to the back of the eye, which can lead to significant and permanent vision impairment. This condition is a considerable global health concern and ranks among the leading causes of irreversible vision loss worldwide.
Distinguishing Pathological Myopia
Pathological myopia is fundamentally defined by the presence of disease-related structural changes in the eye’s posterior segment. High myopia is conventionally defined by a refractive error of -6.00 diopters or greater, or an axial length (eyeball length) exceeding 26.5 millimeters. Pathological myopia typically includes these high measurements, but its true distinction lies in the resulting damage, such as posterior staphyloma or myopic maculopathy.
The underlying mechanism is excessive axial elongation, where the eyeball stretches and grows too long, causing the delicate internal layers to thin and become damaged. This progressive stretching drives the degenerative changes in the retina, choroid, and sclera. The disease is a chronic and degenerative condition, meaning the structural damage tends to worsen over time, regardless of whether the refractive error has stabilized.
Genetic and Structural Risk Factors
The development of pathological myopia is strongly influenced by a genetic predisposition, often running in families with a history of high nearsightedness. While specific gene loci are complex, the pattern of inheritance suggests that the condition is not a random occurrence but is rooted in a person’s biological makeup. The severity of the condition is linked to structural weaknesses in the eye’s outer layer, the sclera.
The sclera and choroid, the layers beneath the retina, possess biomechanical properties that make them susceptible to stretching. As the eye elongates, these layers progressively thin, which leads to the characteristic degenerative changes observed in the posterior pole.
Although genetics sets the stage, environmental factors are thought to accelerate the condition’s progression. Early onset of myopia and the rate of progression in childhood are significant indicators of future risk. Intense near work, such as prolonged reading or screen time, and insufficient time spent outdoors are considered modifiable factors that may worsen the elongation process.
Specific Ocular Complications
The stretching and thinning of the posterior eye wall lead to a cascade of complications. One of the most common and severe is Myopic Macular Degeneration (MMD), which affects the central vision area. MMD begins with structural defects, such as lacquer cracks, which are fine, linear breaks in Bruch’s membrane, a layer supporting the retina.
These cracks can lead to the growth of abnormal, fragile blood vessels from the choroid beneath the retina, known as choroidal neovascularization (CNV). The vessels leak fluid and blood, causing distortion and scarring, which results in central vision loss. Over time, the macula can develop chorioretinal atrophy, where the supporting layers and retina waste away, creating patchy areas of irreparable vision loss.
Another serious complication is retinal detachment, which occurs at a significantly higher rate in eyes with pathological myopia. The stretched peripheral retina becomes thin and weak, often developing degenerative changes like lattice degeneration or small holes and tears. Fluid can then pass through these breaks, causing the retina to peel away from its underlying support.
Glaucoma
Pathological myopia also increases the risk for glaucoma. The structural changes in the elongated eye can alter the drainage angle, making the optic nerve more vulnerable to damage even at pressures considered normal for the general population.
Myopic Traction Maculopathy
The posterior pole can develop myopic traction maculopathy, where the gel-like vitreous humor pulls on the thinned retina. This traction can cause schisis (splitting) or a full-thickness macular hole. The presence of posterior staphyloma, an outward bulging of the thinned sclera, further predisposes the eye to these traction-related issues.
Monitoring and Management Strategies
Regular, specialized eye examinations, including a comprehensive dilated fundus exam, are necessary to track the disease progression. Advanced imaging techniques, such as Optical Coherence Tomography (OCT), provide detailed, cross-sectional views of the retina and choroid, allowing clinicians to detect early signs of fluid, splitting, or neovascularization.
The most effective treatment for myopic CNV involves intravitreal injections of anti-Vascular Endothelial Growth Factor (anti-VEGF) medications. These injections are designed to stop the growth and leakage of the abnormal blood vessels, often stabilizing or improving central vision.
Surgical intervention, specifically pars plana vitrectomy, is the standard approach for treating maculopathy complicated by traction, such as myopic foveoschisis or macular holes. This surgery relieves the pulling forces on the retina caused by the vitreous. Patients are generally advised to avoid activities that increase the risk of eye trauma or sudden jarring, which could potentially trigger a retinal detachment. Early detection and timely treatment of complications are crucial for preserving the best possible visual function.