Even in patients with severe field loss caused by cerebral disease, the macula is spared and central vision persists. Visual field loss caused by retinal detachment begins suddenly, usually in the periphery, and progresses toward the central visual axis over hours to weeks patients may describe this as a dim “shadow” or “curtain.” Field loss caused by stroke or other central nervous system processes is always bilateral, stable, and homonymous, due to crossing of nasal retinal projections at the optic chiasm. However, in 10 to 15 percent of patients with symptomatic posterior vitreous detachment, a retinal flap tear or hole forms as the vitreous pulls away from the retina, especially in the periphery where the retina is thinner ( Figure 2c). 4 Posterior vitreous detachment is harmless by itself, though bothersome floaters (blood or retinal pigment epithelium cells) may develop and persist. Approximately one in four persons develops a posterior vitreous detachment between 61 and 70 years of age, and nearly two thirds have posterior vitreous detachment after 70 years of age. 3 Eventually, the vitreous partly separates from the retinal surface, which is known as posterior vitreous detachment ( Figure 2b). As persons age, this macromolecular network begins to liquefy and collapse, the vitreous shrinks, and vitreo-retinal traction develops. The vitreous humor is a hydrated gel whose structure is maintained by a collagenous and mucopolysaccharide matrix ( Figure 2a). The key pathogenetic steps of rhegmatogenous retinal detachment are illustrated in Figure 2. The third and most common type is rhegmatogenous retinal detachment.
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