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Nutritional and Toxic Optic Neuropathies

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Optic Nerve Disorders

Abstract

Hereditary and acquired metabolic optic neuropathies are both characterized by similar clinical manifestations with preferential involvement of the papillomacular bundle (PMB). PMB fibers are most susceptible to injury as they are small, unmyelinated, and have high energy demands. These optic neuropathies share a presumed common pathophysiology of mitochondrial dysfunction.

Acquired mitochondrial optic neuropathies (MONs) can be categorized into four classes based on etiology: (1) nutritional, (2) drug induced, (3) toxic, and (4) combined metabolic optic neuropathies. Nutritional optic neuropathies, rare in the United States, usually occur with general malnutrition, malabsorption, or alcoholism. The most common nutritional optic neuropathies are due to deficiencies in vitamin B12, folic acid, thiamine, vitamin E, and zinc. A variety of medications cause optic neuropathy by interfering with mitochondrial function. Ethambutol, chloramphenicol, linezolid, erythromycin, streptomycin, and antiretroviral drugs can cause a drug-related MOP especially in genetically predisposed individuals. In many cases, drug toxicity is dose and duration dependent and discontinuation of the drug in a timely manner can lead to significant visual recovery. The most common causes of toxic optic neuropathies are methanol, ethylene glycol, and toluene. Combined nutritional and toxic optic neuropathies have been reported in Cuba, known as the Cuban epidemic of optic neuropathy, tobacco–alcohol amblyopia, prisoners of war, and Strachan’s syndrome.

A number of drugs are associated with optic neuropathy without involving mitochondrial mechanisms such as amiodarone, disulfiram, inferferon-α, infliximab, clomiphene, tamoxifen, and sildenafil. Radiation is also known to induce ischemic optic neuropathy, typically about 18 months after treatment.

MONs are increasingly recognized as a spectrum of conditions that reach a similar end point by compromising a common mitochondrial pathway. Clinicians should be aware of nutritional deficiencies, drugs, and toxins that can cause MON. Prompt recognition of this association is critical in preventing irreversible and profound visual loss.

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Authors and Affiliations

  1. Department of Ophthalmology, Doheny Eye Institute, 1450 San Pablo Street, Los Angeles, California, 90033, USA

    Michelle Y. Wang M.D. & Alfredo A. Sadun M.D., Ph.D.

  2. Department of Neurology, Neuro-Ophthalmology, University of Nevada School of Medicine, 975 Kirman Avenue (111), Reno, Nevada, 89502, USA

    Jane W. Chan M.D.

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    Jane W. Chan

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Wang, M.Y., Sadun, A.A., Chan, J.W. (2014). Nutritional and Toxic Optic Neuropathies. In: Chan, J. (eds) Optic Nerve Disorders. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-0691-4_6

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