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Background: Histological studies on the human optic nerve have documented decreasing axonal nerve fiber counts with age. In patients with optic atrophy, a nonpathological dropout of ganglion cell axons as part of the normal aging process may become clinically significant. Objective: To describe the occurrence of delayed visual loss in patients with presumably “ stable” optic neuropathy. Methods: We reviewed the medical records of 3 patients who experienced slowly progressive visual loss in adulthood after suffering childhood optic nerve injury. Results: All 3 patients had a monophasic illness in childhood that caused bilateral optic atrophy and visual impairment. Following decades of stability, each suffered a gradual, symptomatic visual decline that extended over years. No new ophthalmologic, systemic, or neurologic disorder was found that explained the visual decline in any of these patients. Conclusion: We hypothesize that the late visual decline in these 3 patients resulted from deleterious effects of age-related axonal loss on an already depleted population of neurons.
Background: Histological studies on the human optic nerve have documented increased axonal nerve fiber counts with age. In patients with optic atrophy, a nonpathological dropout of ganglion cell axons as part of the normal aging process may become clinically significant. Objective: To describe the occurrence of delayed visual loss in patients with presumably “stable” optic neuropathy. Methods: We reviewed the medical records of 3 patients who experienced slowly progressive visual loss in adulthood after suffering childhood optic nerve injury. Results: All 3 patients had a monophasic illness in childhood that caused bilateral optic atrophy and visual impairment. Following decades of stability, each suffered a gradual, symptomatic visual decline that extended over years. No new ophthalmologic, systemic, or neurologic disorder was found that explained the visual decline in any of these patients. : We hypothesize that the late visual decline in these 3 patients derived fro m deleterious effects of age-related axonal loss on an already been depleted population of neurons.