Vision loss in toxic and nutritional optic neuropathy is bilateral, symmetric, painless, gradual, and progressive.

Peripheral vision is usually spared since the pattern of loss typically involves a central or cecocentral scotoma, a visual field defect at or surrounding the point of fixation.

[1] Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), halogenated hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol as well as chloroquine and the related hydroxychloroquine (for lupus and rheumatoid arthritis) where it is known as chloroquine retinopathy.

The diagnosis of toxic or nutritional optic neuropathy is usually established by a detailed medical history and careful eye examination.

In most cases of suspected toxic or nutritional optic neuropathy that require neuroimaging, an MRI scan is obtained.

Further testing, guided by the medical history and physical examination, can be performed to elucidate a specific toxin or nutritional deficiency as a cause of the optic neuropathy.

In industrialized nations, toxic and nutritional optic neuropathy is relatively uncommon and is primarily associated with specific medications, occupational exposures, or tobacco and alcohol use disorder.