Developmental stages of dry macular degeneration
Dry AMD can be observed in three phases in both eyes. The stages are determined by a variety of factors.
In this stage, medium-sized drusen are deposited, but there is no change in pigmentation or vision loss. The patient begins with no discernible symptoms at an early stage. If physicians are asked to examine the retina, they will detect tiny white spots known as drusen, which typically develop with advancing age. Reduced retinal cell efficiency makes it challenging to perform tasks and household chores. It is believed that oxidative stress and inflammation induce AMD.
Oxidative stress results from a disruption in the equilibrium between the production of oxygen-containing molecules that interact with other molecules within the cell and the body’s ability to neutralise these molecules.
Antioxidants are molecules that prevent detrimental reactions from occurring. They defend the body against free radicals, and their absence results in oxidative stress.
Oxidative stress is caused by numerous factors, including exposure to glaring light and an insufficiently antioxidant-rich diet. This inflammation contributes to several age-related diseases, such as age-related macular degeneration.
Patients with early AMD maintain excellent vision throughout their lives, whereas those with late AMD experience vision loss.
Intermediate Stage – At this stage, large drusen deposits and pigment variations can be observed. A person with mild vision loss may experience a blurry spot in the centre of their field of vision and may require additional illumination when reading or performing other daily tasks.
Late-Stage – In this advanced stage of AMD, light-sensitive cells and the single supporting tissue in the central retina are destroyed. Geographic atrophy manifests itself in two forms: moist AMD and dry AMD. In this advanced form of dry age-related macular degeneration, there are areas of the retina where cells expire and waste away, known as atrophy, from which the term is derived.
Geographic atrophy results from the demise of photoreceptor cells (light-sensitive cells) and retinal pigment epithelium (PRE) cells. Over time, the area of atrophy spreads to encompass the entire central retina, resulting in the formation of a blind patch in the centre of the visual field.
In some instances, the blurred region will be larger and the individual will have difficulty reading and identifying faces at a distance.
In the desiccated form, choroidal neovascularization (CNV) and blood leakage into the retina are not observed. The disease begins when Brunch’s membrane, another part of the retina, is injured, resulting in the formation of an abnormal blood vessel that can invade the retina as a misguided attempt at healing. The individual may experience visual distortion and diminished central vision in one or both eyes due to the fluid’s immediate and progressive effect on vision.
It is possible for straight lines to appear curved and for blurriness to increase. This form can progress and result in total vision loss without progressing to moist macular degeneration.
