This article includes discussion of toxic and nutritional deficiency optic neuropathies, Cuban epidemic optic neuropathy, drug-induced toxic optic neuropathies, 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. They are usually the 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.
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• Toxic or nutritional optic neuropathy is classically characterized by gradual painless progressive vision loss, bilateral central or cecocentral scotomas, marked dyschromatopsia, loss of high spatial frequency contrast sensitivity, temporal pallor, and loss of papillomacular bundle.
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• Many toxic and nutritional optic neuropathies selectively affect the papillomacular bundle due to a common underlying mitochondrial pathway.
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• A thorough history of medication use, toxic exposure, substance abuse, dietary deficiency, past surgeries, family history, and peripheral neurologic symptoms should be documented.
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• The workup for toxic and nutritional optic neuropathies includes visual field testing, optic coherence tomography, and ancillary laboratory testing tailored to the medical history and examination findings. Magnetic resonance imaging of the brain may be necessary to rule out compressive lesions.
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• Early recognition, removal of toxic agents, and supplementation of nutritional deficiencies may lead to protracted visual recovery.
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 (63). This family of diseases 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) 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 example that illustrates that these multi-factorial conditions have been considered either toxic or nutritional deficiencies 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 (75). 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 (58). The term "tobacco-alcohol amblyopia" suggests the relative roles of cyanide (from tobacco) and low levels of vitamin B12 due to poor nutrition and poor absorption associated with alcohol consumption. Deficiencies of B12, other B vitamins, and folic acid are known causes of a similar clinical picture (18). Indeed, it is one of the fundamental curiosities of these disorders that these nutritional deficiency optic neuropathies, as well as a myriad of toxic optic neuropathies, can have similar clinical manifestations (49).