title: Metabolic optic neuropathies.
abstract: Metabolic optic neuropathies form a rubric of disease characterized by bilaterally symmetrical visual impairment with loss of central visual acuity, dyschromatopsia, centrocecal visual field defects, temporal optic disc atrophy, and specific loss of the nerve fiber layer in the papillomacular bundle. The three subcategories of metabolic optic neuropathies are heredodegenerative (such as Leber's hereditary optic neuropathy), nutritional deficiencies (such as vitamins B12 or folic acid), or toxicities (such as ethambutol or cyanide). It's interesting to note that the first of these three is a congenital cause of mitochondrial impairment, whereas the latter two are acquired injuries to mitochondria. Hence, most if not all causes of metabolic optic neuropathies are, in fact, related to mitochondrial impairment. At the present time there is no effective treatment for heredodegenerative optic neuropathy. Nutritional deficiency metabolic optic neuropathies are treated by giving supplements of the appropriate nutrient or vitamin, whereas toxic metabolic optic neuropathies are treated by removing or preventing exposure to the toxin in question.
authors.affiliation: Department of Ophthalmology, Doheny Eye Institute, University of Southern California, 1450 San Pablo Street, Los Angeles, CA 90033, USA. asadun@hsc.usc.edu
authors.forename: Alfredo A
authors.initials: AA
authors.lastname: Sadun
mesh_terms: D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009748:Nutrition Disorders / Q000150:complications*; D015418:Optic Atrophies, Hereditary / Q000503:physiopathology; D009901:Optic Nerve Diseases / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology