Nutrition-related peripheral neuropathies

Historical note and nomenclature
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By Eduardo Adonias De Sousa MD

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 thiamin 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).