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 patients who have had bariatric surgery (1 General reference Toxic and nutritional optic neuropathies result in reduced visual acuity that is believed to be the result of a destructive reaction in the orbital portion (papillomacular bundle) of the optic... read more ) and those with alcohol use disorder Alcohol Use Disorder and Rehabilitation Alcohol use disorder involves a pattern of alcohol use that typically includes craving and manifestations of tolerance and/or withdrawal along with adverse psychosocial consequences. Alcoholism... read more . True tobacco-induced optic neuropathy is rare. Nutritional optic neuropathy may occur with other nutritional disorders, such as Strachan syndrome (polyneuropathy and orogenital dermatitis).
Lead, methanol, chloramphenicol, digoxin, ethambutol, and many other chemicals can damage the optic nerve. Deficiencies of protein and antioxidants are likely risk factors.
1.Jefferis JM, Hickman SJ: Treatment and outcomes in nutritional optic neuropathy. Curr Treat Options Neurol 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 cause significant central vision loss but not usually complete loss of vision. 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 cecocentral scotomata (caused by involvement of the optic disc and papillomacular fibers) 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 optic neuropathy
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.
Toxic or nutritional optic neuropathy is reduced visual acuity caused most often by drugs or toxins or nutritional deficiencies, particularly in people with alcohol use disorder or in those who have undergone bariatric surgery.
Vision loss is usually gradual and partial, involving central vision.
Diagnosis is mainly clinical (eg, bilateral cecocentral scotomata, suggestive history).
Treat the cause (eg, stopping exposure to a drug or toxin, improving nutrition).
Drugs Mentioned In This Article
|Drug Name||Select Trade|
|AK-Chlor, Chloromycetin, Chloroptic, Chloroptic S.O.P., Ocu-Chlor|
|Digitek , Lanoxicaps, Lanoxin, Lanoxin Pediatric|