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Toxic and Nutritional Optic Neuropathies

(Toxic Optic Amblyopia; Nutritional Optic Amblyopia)


James Garrity

, MD, Mayo Clinic College of Medicine and Science

Last full review/revision Sep 2021| Content last modified Oct 2021
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Toxic and nutritional optic neuropathies result in reduced visual acuity that is believed to be the result of a toxic reaction in the orbital portion (papillomacular bundle) of the optic nerve. It can be caused by various toxic and nutritional factors and probably unknown factors. The main symptom is painless vision loss. Diagnosis is by history and visual field examination. Treatment is avoiding suspected toxic agents and/or improving nutrition.


Toxic or nutritional optic neuropathy is usually bilateral and symmetric. Undernutrition and vitamin deficiencies (eg, vitamins B1 or B12 or folate) may be the cause, particularly in postbariatic surgery patients (1 General reference Toxic and nutritional optic neuropathies result in reduced visual acuity that is believed to be the result of a toxic reaction in the orbital portion (papillomacular bundle) of the optic nerve... read more ) and alcoholics. True tobacco-induced optic neuropathy is rare. Lead, methanol, chloramphenicol, digoxin, ethambutol, and many other chemicals can damage the optic nerve. Deficiencies of protein and antioxidants are likely risk factors. Nutritional optic neuropathy may occur with other nutritional disorders, such as Strachan syndrome (polyneuropathy and orogenital dermatitis).

General reference

  • 1.Jefferis JM, Hickman SJ: Treatment and outcomes in nutritional optic neuropathy. Curr Treat Options Neurol 7;21(1):5, 2019. doi: 10.1007/s11940-019-0542-9

Symptoms and Signs

In patients with toxic or nutritional optic neuropathy, vision blurring and dimness typically develop over days to weeks. An initially small central or pericentral scotoma slowly enlarges, typically involving both the fixation and the blind spot (centrocecal scotoma), and progressively interferes with vision. Color vision may be lost out of proportion to the loss of visual acuity. Total blindness may occur in methanol ingestion, but other nutritional causes typically do not cause profound vision loss. Retinal abnormalities do not usually occur, but temporal disk pallor may develop late.


  • Mainly clinical evaluation

A history of undernutrition, bariatric surgery, or toxic or chemical exposure combined with typical bilateral scotomata on visual field testing justifies treatment. Laboratory testing for lead, methanol, suspected nutritional deficiencies, and other suspected toxins is done.


Patients with decreased vision may improve if the cause is treated or removed quickly. Once the optic nerve has atrophied, vision usually does not recover.


  • Treat the cause of the amblyopia

  • Low-vision aids

The cause of the patient's optic neuropathy is treated. Exposure to toxic substances should stop immediately. Alcohol and other potentially causative chemicals or drugs should be avoided. Chelation therapy is indicated in lead poisoning. Dialysis, fomepizole, ethanol, or a combination is used for methanol poisoning. Treatment with oral or parenteral B vitamins and/or folate before vision loss becomes severe may reverse the condition when undernutrition is the presumed cause.

Low-vision aids (eg, magnifiers, large-print devices, talking watches) may be helpful.

The role of antioxidants has not been fully characterized. Their use could be justified on a theoretic basis; however, there is no proof of efficacy, and the at-risk population that should receive such supplements has not been defined.

Key Points

  • Toxic or nutritional optic neuropathy is reduced visual acuity caused most often by drugs or toxins or nutritional deficiencies, particularly in alcoholics or in those who have undergone bariatric surgery.

  • Vision loss is usually gradual and partial.

  • Diagnosis is mainly clinical (eg, bilateral scotomata, suggestive history).

  • Treat the cause (eg, stopping exposure to a drug or toxin, improving nutrition).

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