Toxic and nutritional deficiency optic neuropathies

Peter A Quiros MD (Dr. Quiros of the Doheny Eye Center UCLA and the David Geffen School of Medicine has no relevant financial relationships to disclose.)
Jonathan D Trobe MD, editor. (Dr. Trobe of the University of Michigan has no relevant financial relationships to disclose.)
Originally released August 4, 1997; last updated January 19, 2015; expires January 19, 2018

This article includes discussion of toxic and nutritional deficiency optic neuropathies, Cuban epidemic optic neuropathy, drug-induced retrobulbar toxic optic neuropathies, Jamaican optic neuropathy, nutritional deficiency optic neuropathies, tobacco-alcohol amblyopia, toxic optic neuropathies, and tropical amblyopia. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Toxic and deficiency optic neuropathies are fairly uncommon in the United States. Nonetheless, they are seen in a subset of patients, usually as a result of drug toxicity. Due to the effects of these conditions on mitochondria and cellular energy production, these entities share many signs and symptoms. Awareness of the hallmark findings of these entities as well as an increased index of suspicion in patients with chronic disease will assist the clinician with diagnosis of these too easily missed cases of unexplained vision loss.

Historical note and terminology

Toxic and nutritional optic neuropathies are uncommon in the United States. However, in some times and places these types of optic neuropathies have been far more common; they took on epidemic proportions in Cuba in the early 1990s (Sadun et al 1994a). This family of diseases, hence, tends to be relegated to the background until such events as famine, new application of pharmaceuticals, or changes in the workplace health and living conditions lead to nutritional deficiencies or toxic exposures.

Ordinarily, these entities are divided into nutritional (deficiency states) neuropathies and toxic neuropathies. But many are multi-factorial, a clear etiology cannot be established, and the terms are often used presumptively. There is no doubt, however, that as the number of new drugs and chemicals increases, more toxic-metabolic optic neuropathies will be identified. One well-known entity that illustrates that this multi-factorial disease may be considered toxic or nutritional deficiency is "tobacco-alcohol amblyopia." This entity was first well described by Traquair, who emphasized the slowly progressive time course of the bilateral visual field loss (Traquair 1930). The etiologic factors in tobacco-alcohol amblyopia are now better appreciated, even as there has been a marked decrease in the prevalence of the condition in the United States (Rizzo and Lessell 1993). The term "tobacco-alcohol amblyopia" suggests the relative roles of cyanide (from the tobacco) and low levels of vitamin B12 due to poor nutrition and poor absorption associated with alcohol consumption. Deficiencies of B12 as well as other B vitamins and, folic acid in particular, are known causes of a similar clinical picture (Golnik and Schaible 1994). Indeed, it is one of the fundamental curiosities of these disorders that these deficiencies as well as a myriad of toxic optic neuropathies can all have similar characteristic clinical manifestations (Newman 1996).

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