The retina is a thin, multi-layered sheet of light-sensitive tissue lining the back of the eye, functioning like a camera sensor. It receives light focused by the lens, converts it into neural signals via specialized photoreceptor cells, and transmits those signals to the brain through the optic nerve. As an extension of the central nervous system, the retina is highly metabolically active and vulnerable to damage, which can lead to rapid and permanent vision loss. Retinal abnormalities affect the tissue’s physical structure, blood supply, or genetic integrity.
Structural Abnormalities of the Retina
Structural abnormalities involve the physical displacement, tearing, or alteration of the retina’s tissue layers. The retina’s integrity relies on its adherence to the underlying retinal pigment epithelium (RPE); separation compromises function.
The most common form is rhegmatogenous retinal detachment, caused by a full-thickness tear or break (“rhegma”) in the neurosensory retina. Liquefied vitreous gel passes through this break, accumulating in the subretinal space and separating the retina from the RPE. This separation deprives photoreceptors of oxygen and nutrients supplied by the underlying choroid, causing rapid vision loss in the affected area.
Epiretinal membranes (ERMs), also known as macular pucker, are scar tissue that grows on the inner retinal surface. This tissue is composed of cells, such as glial cells, that migrate onto the surface, often following age-related separation of the vitreous gel. As the membrane contracts, it wrinkles the underlying retina, causing distortion and blurring of central vision.
Macular holes are full-thickness defects developing in the fovea, the center of the macula responsible for sharp central vision. They are caused by abnormal vitreous traction, where the shrinking vitreous gel pulls forcefully on its attachment point. This mechanical tugging tears the delicate retinal tissue, creating an open defect that severely impairs central sight.
Vascular Abnormalities of the Retina
Vascular abnormalities affect the intricate network of arteries and veins that supply the inner retina with oxygen and nutrients. Because these vessels are small, they are susceptible to damage from systemic diseases like diabetes and high blood pressure.
Diabetic retinopathy is a progressive condition where chronic high blood sugar damages retinal blood vessels. The early phase, non-proliferative diabetic retinopathy (NPDR), involves the formation of microaneurysms—tiny bulges in vessel walls that leak fluid and blood into the retina. As the disease advances, widespread vessel blockage reduces blood flow, causing the retina to become oxygen-deprived (ischemia).
The retina responds to this lack of oxygen by releasing growth factors that stimulate the advanced stage: proliferative diabetic retinopathy (PDR). PDR involves neovascularization, the growth of fragile, abnormal new blood vessels on the retinal surface. These new vessels are prone to rupture, causing severe hemorrhages and forming scar tissue that can pull on the retina, potentially causing tractional retinal detachment.
Retinal artery and vein occlusions, often called “eye strokes,” involve a sudden blockage of a retinal blood vessel. A retinal artery occlusion (RAO) occurs when an embolus (a small clot or cholesterol plaque) lodges in the central retinal artery or a branch, immediately cutting off oxygen supply to the inner retina. This lack of oxygen causes rapid vision loss, making it a time-sensitive emergency.
Conversely, a retinal vein occlusion (RVO) results from a blockage, typically a blood clot, in a retinal vein, preventing deoxygenated blood from draining. The resulting pressure buildup causes blood and fluid to spill into the retinal tissue, leading to swelling, hemorrhages, and sudden blurring or loss of vision. RVOs are associated with systemic high blood pressure and other cardiovascular risk factors.
Degenerative and Inherited Retinal Conditions
This category includes conditions defined by the gradual, chronic breakdown of retinal cells, often driven by age-related changes or genetic errors. These processes result in a progressive loss of function rather than an acute structural or vascular event.
Age-related Macular Degeneration (AMD) is the leading cause of irreversible central vision loss in older adults. The dry form, accounting for about 90% of cases, is characterized by the slow accumulation of yellowish deposits called drusen beneath the retina. Drusen are composed of cellular waste material and lead to the thinning and atrophy of the retinal pigment epithelium and overlying photoreceptors, resulting in gradual central vision loss.
The less common but more severe wet form of AMD often develops from the dry form. In wet AMD, an abnormal signal cascade, involving vascular endothelial growth factor (VEGF), triggers the growth of new, fragile blood vessels from the choroid into the subretinal space. This process, called choroidal neovascularization, causes the vessels to leak fluid and blood, rapidly damaging the macula and leading to acute visual distortion and central vision loss.
Retinitis Pigmentosa (RP) is a group of inherited disorders caused by mutations in genes necessary for photoreceptor function. The disease begins with the progressive death of rod photoreceptors, which are responsible for low-light vision. This leads to early symptoms of night blindness and a gradual constriction of the peripheral visual field, often described as “tunnel vision.” Cones, responsible for central and color vision, die off secondarily, leading to eventual loss of central acuity. This degeneration is chronic and progressive.