Overview
Toxic optic neuropathies (TON) occurs following exposure to a toxin (for example, certain drugs, alcohol or tobacco use and certain systemic medications). It is characterised by temporal disc pallor due to damage to the retinal ganglion cell axons within the papillomacular bundle. OCT will show temporal RNFL thinning and visual fields often present with a central or centrocaecal scotoma.
Symptoms include a painless progressive and bilateral reduction of vision. Colour vision may also be affected.
Some common causes of TON include ethambutol, methanol, tobacco and alcohol. Amiodarone may cause a prolonged bilateral disc swelling with bilateral vision loss, followed by optic atrophy.
Management is the removal of the toxic agent (to be done in consultation with the patient's health care professionals especially if the TON has been caused by a prescribed mediation). Damage that has occurred due to TON may recover to some degree, however this is not always the case and some TON related to systemic medications may continue to worsen even after the cessation of the medication.
Nutritional optic neuropathies present similarly to TON but is caused by deficiencies in dietary intake including vitamin B12, folic acid and copper deficiencies.
Case Examples
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Case 1
A 55 year old Caucasian male with best corrected visual acuity of 6/7.5 (20/25) in each eye. He has a strong history of alcoholism and smoking.
Based on the patient history and clinical findings below, the working diagnosis for this patient is toxic/nutritional neuropathy.
References
Grzybowski, A., Zülsdorff, M., Wilhelm, H. and Tonagel, F. (2015), Toxic optic neuropathies: an updated review. Acta Ophthalmol, 93: 402-410.
Sharma, P., & Sharma, R. (2011). Toxic optic neuropathy. Indian journal of ophthalmology, 59(2), 137–141.