Reticular degeneration, often referred to as lattice degeneration, is a common, asymptomatic alteration affecting the peripheral retina. This condition involves abnormal thinning of the neurosensory tissue, the light-sensitive layer at the back of the eye. While the degeneration itself does not cause immediate vision loss, it substantially increases the risk of rhegmatogenous retinal detachment. Its presence necessitates regular, careful examination to prevent potential vision-threatening events.
The Structure and Location of Reticular Degeneration
Reticular degeneration is strictly confined to the far periphery of the retina. It is characterized by distinct, sharply demarcated patches of retinal thinning that are typically oval or elongated. These lesions often appear as a net-like or lattice pattern, giving the condition its alternate name.
Within these thinned areas, blood vessel sclerosis occurs, where the vessels become hardened and appear as fine, branching, white or gray lines. This visible network of sclerotic vessels and surrounding retinal atrophy creates the characteristic physical appearance. The condition is common, found in approximately 6% to 10% of the general population, and is often bilateral, affecting both eyes.
The underlying vitreous gel over the area of degeneration tends to become liquefied, a process called synchysis. This localized liquefaction and poor adhesion contribute to the structural instability of the lesion. Pigment clumps may also be present, indicating chronic damage to the underlying retinal pigment epithelium. The lesions can evolve over time, sometimes resulting in the development of small, round, full-thickness holes within the thinned retina.
Recognizing Early Warning Signs
The reticular degeneration lesions typically produce no symptoms because they are located in the far peripheral vision and do not affect central sight. However, symptoms that arise are usually warning signs of an associated complication, such as a retinal tear or a posterior vitreous detachment (PVD). An acute PVD, the separation of the vitreous gel from the retinal surface, often precipitates a tear in a weakened area of degeneration.
Patients may suddenly notice new floaters—small specks, strings, or cobweb-like shapes that drift across the field of vision. These floaters are caused by cellular debris and condensed vitreous fibers that become visible as the vitreous gel separates. Another common complaint is photopsia, the perception of flashing lights or streaks of light, particularly in the peripheral vision.
These flashes occur when the separating vitreous gel pulls or tugs on the retina, stimulating the photoreceptor cells. A sudden increase in the number or size of floaters, or the onset of persistent flashes, indicates mechanical traction is occurring and requires immediate ophthalmic evaluation.
The Mechanism of Retinal Detachment
The primary concern is the propensity of reticular degeneration to lead to a rhegmatogenous retinal detachment. This process begins with the natural aging of the vitreous gel, which gradually shrinks and liquefies, leading to eventual Posterior Vitreous Detachment (PVD). In eyes with reticular degeneration, the retina is abnormally thin and firmly adherent to the vitreous at the margins of the lattice patch.
As the vitreous gel pulls away during a PVD, this strong localized adhesion can exert mechanical force, causing the retina to tear. These tears are often horseshoe-shaped or flap tears. Alternatively, chronic thinning within the lesion can lead to the formation of atrophic holes, which are full-thickness defects occurring without significant vitreous traction.
Once a tear or hole is created, the liquefied vitreous fluid can pass through this opening and accumulate between the neurosensory retina and the underlying retinal pigment epithelium (RPE). This fluid buildup overcomes the natural forces that keep the retina attached to the RPE layer. The accumulation of fluid physically peels the retina away from its nourishment source, resulting in a retinal detachment.
The detachment typically begins in the periphery and progresses inward, leading to a visible shadow, veil, or curtain effect in the field of vision. If the detachment is not repaired promptly, the retina will be separated from its blood supply and cease to function, resulting in permanent vision loss.
Clinical Diagnosis and Management Strategies
The diagnosis of reticular degeneration relies on a comprehensive, dilated eye examination performed by an eye care specialist. Dilating drops are used to widen the pupil, allowing the doctor to use indirect ophthalmoscopy to view the far peripheral retina. Scleral depression may also be used, where gentle pressure is applied to the outside of the eye to bring the peripheral tissue into better view.
Once identified, the management strategy is determined by the presence or absence of associated retinal breaks and symptoms. For patients with asymptomatic reticular degeneration that does not contain holes or tears, the standard approach is monitoring through regular follow-up examinations.
If the degeneration is deemed high-risk, such as when a retinal tear or a symptomatic atrophic hole is present, prophylactic treatment may be recommended to prevent detachment. The most common procedure is laser photocoagulation, which uses a focused laser beam to create tiny burns around the edges of the lesion or break.
These burns heal into a scar, creating a strong adhesive barrier that “spot welds” the retina to the underlying tissue. Another prophylactic option is cryotherapy, or freezing treatment, which achieves the same scarring and adhesion effect using a cold probe applied to the external eye surface. Both laser and cryotherapy circumferentially wall off the weakened area, preventing liquefied vitreous fluid from passing under the retina and mitigating the risk of a progressive retinal detachment.