Nutritional and toxic optic neuropathies (NTON)

Optic nerve damage due to nutritional deficit or a toxin.

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Aetiology

Nutritional optic neuropathy (NON):

Nutritional optic neuropathy is usually sporadic; however, it has been described as epidemic during the times of war and/or famine.

• B12-deficiencies (M/C NON)
• Folate deficiencies
• Copper deficiencies

Toxic Optic Neuropathy (TON):

Use of toxic mediacations as well as injestion or inhalation of toxic substances can both cause toxic optic neuropathy.

• CLAIMED
  • Chloramphenicol, cyanide (component of tobacco)
    • Chronic use of alcohol in heavy smokers (M/C overall)
  • Lead
  • Aspirin, arsenic, alcohol, amiodarone
  • Isoniazid
  • Methanol optic neuropathy (acute presentation)
  • Ethambutol (antimycobacterial drug)
  • Digoxin

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Clinical features

Toxic and nutritional optic neuropathies both present clinically with symmetric progressive bilateral vision loss, decreased color vision, central or cecocentral scotomas on formal visual field testing, and no relative afferent pupillary defect because of the symmetric nature of optic nerve involvement.

• Diminution of vision: bilaterally symmetrical, painless, gradually progressive
• Dyschromatopsia

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Diagnosis

Ophthalmoscopic examination:

• Pupils: sluggish, no RAPD
• Optic disc: normal, swollen, or hyperemic in early stages, temporal optic disc pallor later
• Visual field defect: centrocaecal scotoma