Nutrition-related peripheral neuropathies

Matthew Varon MD (

Dr. Varon of the University of Kansas Medical Center has no relevant financial relationships to disclose.

Mamatha Pasnoor MD (

Dr. Pasnoor of the University of Kansas Medical Center received medical advising fees from Alexion Pharmaceuticals, CSL Behring, and TerumoBCT and a consulting fee from Momenta Pharmaceuticals.

Constantine Farmakidis MD (

Dr. Farmakidis of the University of Kansas Medical Center received consulting fees from Terumo BCT and Momenta.

Mazen M Dimachkie MD (

Dr. Dimachkie, Director of the Neuromuscular Disease Division and Executive Vice Chairman for Research Programs, Department of Neurology, The University of Kansas Medical Center, received honorariums from Alnylam, Audentes, Baxalta, Catalyst, CSL Behring, Mallinckrodt, Momemta, Novartis, NuFactor, Sanofi, Shire, RMS Medical, and Terumo for speaking engagements or consulting work, and grants from Alexion, Alnylam, Amicus, Biomarin, BMS, Catalyst, CSL Behring, FDA/OPD, Genentech, Genzyme, GlaxoSmithKline, Grifols, MDA, Novartis, Octapharma, Orphazyme, Sanofi,TMA, UCB BioPharma, and Viromed.

Louis H Weimer MD, editor. (

Dr. Weimer of Columbia University has received consulting fees from Roche.

Originally released November 2, 1999; last updated January 16, 2019; expires January 16, 2022

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 neuropathies include neuropathies that result from either vitamin or mineral deficiency or toxicity. These disorders are usually related to acquired factors, such as deficiency states from either a 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 multisystem 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). There were several reports of multisystem polynutritional neurologic syndromes closely resembling Strachan syndrome in Canadian prisoners of war and in Cuba in the early 1990s (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 or even lesser amounts) can precipitate an acute sensory neuropathy over several weeks (Schaumburg et al 1983). In a series of 13 patients with acute axonal nutritional neuropathy from either bariatric surgery, alcohol abuse, or chronic vomiting, all 13 were found to have low thiamine levels. All patients experienced some improvement from treatment with greater improvement in motor than sensory deficits (Hamel and Logigian 2018).

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. Overall, however, response to nutritional supplementation is highly variable. Supportive measures are discussed in Peripheral neuropathies: supportive measures and rehabilitation.

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 had chronic nutritional neuropathic syndromes, including optic atrophy and sensory peripheral neuropathy.

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