![]() ![]() (b) Optical coherence tomography angiography image of the same patient showing the branching network of vessels of the choroidal neovascular membrane with a surrounding dark halo. (a) Fundus image of a myopic patient showing a grayish lesion at the fovea with pigmented margins, suggestive of a choroidal neovascular membrane. They appear as well-defined areas of hyperfluorescence in the early phase with progressive leakage of dye in the late phases of the angiogram. Myopic CNV are predominantly classic type on fluorescein angiography. OCT shows a hyper-reflective-elevated lesion in the subretinal space, usually without much exudative changes such as fluid under the neurosensory retina or intraretinal edema. Fluorescein angiography, indocyanine green angiography, OCT, and OCTA are helpful in confirming the diagnosis. As the retina is thin, bleeding does not usually obscure these lesions and they are easily visible on clinical examination. It appears as a grayish subretinal membrane with hyperpigmented borders. Myopic CNV develops in 10% of high myopes and 30% myopes eventually develop CNV in the other eye as well. Macular CNV is a one of the most common complications that results in reduced central vision in patients with PM. The presence of pigment abnormalities, abnormal autofluorescence, and abnormal reflectance in infrared imaging, performed using wide field imaging systems such as Optos ™, have been proposed as markers to identify the edge of the staphyloma. A newer classification of staphylomas based on three-dimensional magnetic resonance imaging and ultrawide field imaging has also been proposed. The normal choroidal flush is absent in a high percentage of posterior staphylomas, suggesting the possibility of ischemia which may further lead to development of a CNV in these eyes. The eyes with shallow staphylomas show a larger drop in VA and a greater occurrence of CNV and macular hemorrhage. Posterior staphyloma formation is further linked to development of myopic maculopathy. Its incidence increases with age, occurring mostly after the fifth decade. There are ten different types of staphyloma according to Curtin. It is seen as a secondary depression with bending of vessels at the margin and a dark crescentic nasal reflex. Spaide defined a posterior staphyloma as “outpouching of the wall of the eye that has a radius of curvature less than the surrounding radii of curvature.” The best way to diagnose a posterior staphyloma is by an indirect ophthalmoscope, which gives a stereoscopic view of the fundus. It is an outward protrusion of all coats of the posterior pole and is considered pathognomonic of PM. Posterior Staphyloma (Scarpa's Staphyloma) This discrepancy in receptor alignment is directly associated with the axial length. In high myopes, the cones in nasal hemiretina are aligned toward the optic nerve, whereas they are aligned toward the center of the exit pupil in temporal hemiretina. This may lead to subnormal visual function (Stiles–Crawford effect). The arrangement of the photoreceptors in high myopes is affected due to excessive stretch in the posterior pole. One of the reasons behind this may be the alteration in the arrangement of photoreceptors. Visual acuity (VA) in HM may be subnormal even before advanced myopic maculopathy sets in. Furthermore, scleral thinning may cause deformation of the posterior pole leading to staphyloma formation with a shorter radius of curvature. Thinned out chorioretinal tissue is associated with poor blood circulation and may lead to CNV development by inducing vascular endothelial growth factor (VEGF) expression. Myopia-related complications such as posterior staphyloma and chorioretinal atrophy increase proportionally with increase in axial length. The amacrine cells of the retina are thought to play a critical role in this chain of molecular signaling, initiated due to a retinal defocus, which leads to alteration of refractive error. There may exist a chain of molecular signals arising from the retina which modulate the changes in thickness of the choroid and the scleral growth. As a consequence of defocus, choroid thickening or thinning occurs, moving the retina toward the plane of focus. Studies have hypothesized the role of choroid in ocular elongation in response to retinal defocus. Abnormal collagen proteins may lead to degenerative changes in the retina, choroid, and sclera. The mechanism behind pathological axial elongation includes an emmetropization process and involves a structural alteration of the collagen proteins. Axial elongation results in chorioretinal stretching and subsequent thinning. To begin with, there occurs excessive axial elongation. Pathological changes in high myopes start in childhood and become prominent in adulthood. ![]()
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