BASICS

DESCRIPTION

• Painless, bilateral vision loss including dyschromatopsia and central or centrocecal scotoma

• Exception is unilateral vision loss from phosphodiesterase inhibitors, which are possibly associated with ischemic optic neuropathy

• Typically slowly progressive; less often acute

– Toxins [e.g., methanol, ethylene glycol, toluene, styrene, carbon monoxide, cyanide (from smoking and cassava)]

– Drugs

– Direct (e.g., ethambutol, disulfiram iodochlorohydroxyquinoline, alpha interferon, vincristine, amiodarone, cyclosporine, tacrolimus)

– Indirect (phosphodiesterase inhibitors and infliximab)

– Nutritional deficiencies (e.g., vitamin B12, thiamine, folate)

• System(s) affected: Nervous

EPIDEMIOLOGY

• Affects all ages, races, and economic strata

• Both sexes are equally affected

• Nutritional affects individuals from lower economic status and during times of war and famine

• More common in individuals on certain drugs, occupational exposure, smokers, and alcoholics

Incidence

• Varies on type, yet not known in most cases

– Ethambutol optic neuropathy is 1.5% in 1 Korean study or 100,000 new cases annually (1)

Prevalence

Unknown but varies with type

RISK FACTORS

• Impaired renal disease with ethambutol

• Occupational exposure for toluene and styrene

• Smoking with toxic and nutritional causes

– Pipe and cigar more than cigarettes

• Alcohol intake is often associated with nutritional causes

Genetics

Unknown

GENERAL PREVENTION

• Regular monitoring of patients on ethambutol

• B-complex vitamins and vitamin A reduces incidence in Cuba

PATHOPHYSIOLOGY

• Generally related to interference of mitochondrial function with oxidative stress

– Demyelination of white matter—formic acid, a metabolite of methanol, is a mitochondrial toxin

– Defective mitochondrial oxidative phosphorylation, with buildup of reactive oxygen species in the optic nerve in ethambutol and Cuban epidemic optic neuropathy

– Chelates metal-containing enzymes used in the mitochondria with ethambutol, disulfiram, and penicillamine

– Smoking may cause elevated cyanide

• Vascular changes at optic nerve head with phosphodiesterase inhibitors

ETIOLOGY

Multifactorial with both poor nutrition and toxicity playing roles

COMMONLY ASSOCIATED CONDITIONS

• Smoking and alcohol use are seen often but are not clearly demonstrated

– Tobacco may be a toxin by itself

– Alcohol is not a primary contributor; but is related to poor nutrition

• Pernicious anemia with vitamin B12 deficiency

DIAGNOSIS

HISTORY

• Either acute (some nutritional and toxins) versus gradual progressive loss of color and central vision

– Careful documentation of exposure to drug or toxin or dietary history (2)[B]

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