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Pyridoxine excess
Toxic doses of pyridoxine may also result in a large fiber sensory peripheral neuropathy(Schaumburg et al 1983; Parry and Bredesen 1985; Dalton and Dalton 1987). Mega doses ofpyridoxine may produce a sensory neuropathy after several weeks of use, generally in excess of 2grams per day. It has also been reported with longstanding use of as little as 200 mg a day.

Symptoms of paresthesias, ataxia, and burning feet occur 1 month to 3 years after startingpyridoxine.
Axonal degeneration, reduced myelin fiber density, and myelin debris have all been demonstratedin sural nerve biopsies. After stopping the pyridoxine, few patients entirely resolved, but mostimproved. Individuals who use large doses of B-complex vitamins are under the false impressionthat, because B-complex vitamins are water soluble and, therefore, are excreted in the urine, it isnot possible to take too much. In fact, 200 mg doses of pyridoxine are commonly found assingle tablets in pharmacies and are sufficient to cause a sensory neuropathy after many months of exposure.

Strachan's syndrome
In 1888, Henry Strachan, a British medical officer stationed in Jamaica, described a syndrome of painful peripheral neuropathy, ataxia, optic neuropathy, and stomatitis among sugarcane workers (Strachan 1897). Denny Brown and others found similar ailments among allied troops liberated from prisoner of war camps after World War II (Denny-Brown 1947).

Other symptoms included sensorineural deafness, dizziness, confusion, spastic leg weakness, foot drop, Wernicke's encephalopathy, and rare cases of neck extensor weakness and myasthenic bulbar weakness. Poor nutrition, hard physical labor, and concurrent infection were thought to be exacerbating factors.
Fischer performed autopsies on a series of Canadian prisoners of war, the most prominent pathologic findings were demyelination of the posterior columns of thoracic and cervical spinalcord (Fischer 1955).
More recently, an outbreak of optic and peripheral neuropathy closely resembling Strachan's syndrome occurred in Cuba from 1992 to 1993 following a loss of food and fuel imports from the former Soviet Union (Roman 1994). Fifty thousand people developed either isolated or combined optic neuropathy, painful sensory neuropathy, dorsal lateral myelopathy, sensory neural deafness, spastic paraparesis, dysphonia, and dysautonomia. Forty- five percent developed centrocecal scotoma and optic neuropathy only, often following a period of weight loss. A number of possibilities were proposed, including vitamin B-complex and thiamin deficiency, cyanide intoxication, viral infections, and mitochondrial deletions. Heavy alcohol and tobacco use were found most frequently in those with optic neuropathy (tobacco-alcohol amblyopia). Clinical evidence of neuropathy was often lacking despite the severe symptoms (Thomas et al 1995).Sural nerve biopsy showed axonal degeneration of large myelinated fibers. Most patients responded to supplementation of B-complex vitamins.