in both eyes in addition to experiencing pain in their extremities and hearing loss. Their visual loss did not correlate well with malnutrition and that not all prisoners experienced the loss of vision. Toxic optic neuropathies (TON) Toxic optic neuropathy refers to the ingestion of a toxin or an adverse drug reaction that results in vision loss from optic nerve damage. Patients may report either a sudden loss of vision in both eyes, in the setting of an acute intoxication, or an insidious asymmetric loss of vision from an adverse drug reaction. The most important aspect of treatment is recognition and drug withdrawal. Among the many causes of TON, the top 10 toxins include: Medications Ethambutol, rifampin, isoniazid, streptomycin (tuberculosis treatment) Linezolid (taken for bacterial infections, including pneumonia) Chloramphenicol (taken for serious infections not helped by other antibiotics) Isoretinoin (taken for severe acne that fails to respond to other treatments) Ciclosporin (widely used immunosuppressant) Acute Toxins Methanol (component of some moonshine, and some cleaning products) Ethylene glycol (present in anti-freeze and hydraulic brake fluid) Metabolic disorders may also cause this version of disease. Systemic problems such as diabetes mellitus, kidney failure, and thyroid disease can cause optic neuropathy, which is likely through buildup of toxic substances within the body. In most cases, the cause of the toxic neuropathy impairs the tissue's vascular supply or metabolism. It remains unknown as to why certain agents are toxic to the optic nerve while others are not and why particularly the papillomacular bundle gets affected. Combined Mitochondrial Optic Neuropathies Tobacco Alcohol Ambylopia (TAA) TAA is an old term for a constellation of elements that can lead to a mitochondrial optic neuropathy. The classic patient is a man with a history of heavy alcohol and tobacco consumption. Respectively, this combines nutritional mitochondrial impairment, from vitamin deficiencies (folate and B-12) classically seen in alcoholics, with tobacco-derived products, such as cyanide and ROS. It has been suggested that the additive effect of the cyanide toxicity, ROS, and deficiencies of thiamine, riboflavin, pyridoxine, and b12 result in TAA. Cuban Epidemic of Optic Neuropathy Between 1992 and 1993, in the Cuban Epidemic of Optic Neuropathy, nearly 50,000 people in Cuba were affected with optic neuropathy, sensory and autonomic peripheral neuropathy, neural deafness, and in a few cases, myelopathy. The most common pattern of symptoms consisted of severe weight loss, fatigue and a subacute loss of vision. On the fundus,