This article includes discussion of nutrition-related peripheral neuropathies and alcohol-induced neuropathies. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Nutrition-related disorders primarily include vitamin or mineral deficiency or toxicity. Hereditary causes are rare. These disorders are usually related to acquired factors, such as deficiency states stemming from lack of nutrient intake or malabsorption from gastrointestinal etiology. The discovery and isolation of vitamins and their relation to neuropathy began with the study of beriberi in the 19th century. Although beriberi has been recognized for centuries, the disease reached epidemic proportions during the Industrial Revolution, when grain mills began producing polished rice, mechanically stripping off the nutrient-rich husk. Epidemics of painful polyneuropathy and heart failure broke out in regions where rice was the major source of carbohydrate, particularly in Asia. In 1897, Eijkman reproduced neuropathy in pigeons by feeding them polished rice and then cured the disease with crude unpolished rice. An intense search began for the antineuritic factor within the rice husks. Funk first coined the term "vitamine" in 1911, thinking that this was the anti-beriberi factor within the rice extracts, later discovered to be nicotinic acid amide (niacin). The anti-beriberi factor was discovered in 1936, and the name was changed to thiamine to reflect the molecule's sulfur content (Victor 1984; Kinsella and Riley 1998).
The history of the role of nutrition and its relation to peripheral neuropathy is a rich one. Denny-Brown conducted a detailed analysis of patients with burning feet and other maladies associated with prisoner-of-war camps in Japan and the Far East during World War II (Denny-Brown 1947). Victor, through his study of Wernicke-Korsakoff syndrome, recognized a high prevalence of neuropathy in chronic alcoholics (Victor 1984). Strachan, a British medical officer, identified a polynutritional disturbance in Jamaican sugarcane workers in 1898 that was characterized by sensorineural hearing loss, optic and peripheral neuropathy, corticospinal tract dysfunction, and ataxia (Strachan 1897). Later, Fischer described the pathologic features of Strachan syndrome in Canadian prisoners of war, years after their initial nutritional insult in the Far East during World War II (Fischer 1955). An outbreak of polyneuropathy and optic neuropathy occurred in Cuba in 1992 and 1993 following the collapse of Soviet food supports, which was identified to be polynutritional in etiology, closely resembling Strachan syndrome (Borrajero et al 1994; Roman 1994; Thomas et al 1995).
Nutritional neuropathies are usually slowly progressive; however, there are situations in which the onset of the neuropathic symptoms may be acute or subacute (Weber et al 1990). Alcoholic neuropathy may deteriorate suddenly in a Guillain-Barré-like fashion (Wohrle et al 1998). In patients who are vitamin B12 deficient, a single exposure to nitrous oxide may precipitate within days to weeks a syndrome of paresthesias in the feet and hands and classic myeloneuropathy (Flippo and Holder 1993; Kinsella and Green 1995). Following gastric restriction procedures for weight loss, individuals may develop a severe debilitating axonal neuropathy within weeks following unremitting vomiting (Peltier et al 1979; Feit et al 1982; Paulson et al 1985; Somer et al 1985; Harwood et al 1987). Large doses of pyridoxine (2000 mg every day) can precipitate an acute sensory neuropathy over several weeks (Schaumburg et al 1983).
Most nutritional deficiency syndromes are similar in that they are all potentially reversible if recognized early. The longer diagnosis is delayed, the less likely the patient will have complete, or even significant, improvement.
Robson and colleagues performed a follow-up study of prisoners of war who suffered malnutrition in Far East prison camps during World War II (Robson et al 2009). They found excess mortality due to infections, suicide, and cirrhosis, possibly from hepatitis B exposure. About 5% of the survivors have chronic nutritional neuropathic syndromes, including optic atrophy and sensory peripheral neuropathy.
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