Toxic / Nutritional Optic Neuropathy

DOS Times Vol. 11, No. 8 February, 2006 These disorders are often grouped together as they cause a syndrome characterized by papillomacular bundle damage, central or cecocentral scotoma, and reduction of color vision. The anterior visual pathway is susceptible to damage from toxins or nutritional deficiency (Table 1). Both toxicity and malnutrition, acting either independently or together, have been implicated in the pathogenesis of these disorders. Ethambutol is one drug that is commonly is associated with toxic optic neuropathy. The optic neuropathy that occurs is dose dependent and duration related. Loss of vision does not tend to occur until the patient has been on the drug for at least 2 months, but symptoms generally appear between 4 months to a year. This onset may be sooner if the patient has concurrent renal disease because this will result in reduced excretion of the drug and, therefore, elevated serum levels. The toxicity of this drug is dose related. The patients on dosages of 25 mg/kg/d or greater are most susceptible to vision loss. However, cases of vision loss, even with much lower doses, have been reported. Isoniazid, another antitubercular drug, also can produce toxic optic neuropathy, and patients with concurrent hepatic or renal disease are at higher risk. Amiodarone, an anti arrhythmic drug has been implicated as a cause of an optic neuropathy. Its most common ocular side effect is verticillate keratopathy. Although the optic neuropathy is typically bilateral and symmetric with visual loss and/or field loss, it also may present unilaterally. With this drug, the toxicity to the optic nerve also appears to be dose related, with dosage varying from 200-1200 mg/ d. Visual complaints may start 1-72 months after the initiation of treatment and are slowly progressive. The optic neuropathy from amiodarone, should not be confused with the acute nonarteritic ischemic optic neuropathylike picture also reported with this drug.