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.

)
Constantine Farmakidis MD (

Dr. Farmakidis of the University of Kansas Medical Center received consulting fees from Argenx.

)
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 14, 2020; expires January 14, 2023

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.

Overview

Nutrition-related neuropathies include neuropathies that result from either vitamin or mineral deficiency or toxicity. Vitamins and minerals that are most important for peripheral nerve function include the B vitamins (B1, B6, folate, and B12), vitamin E, and copper, the mineral. Early identification of these entities is important as their clinical course may be stabilized or reversed by adequate treatment.

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, at which time the disease had reached epidemic proportions as a result of the Industrial Revolution. Epidemics of painful polyneuropathy and heart failure broke out in regions where rice was the major source of carbohydrate. In 1897, Eijkman observed that chickens fed polished rice developed beriberi and were then cured when fed crude unpolished rice. The anti-beriberi factor was finally discovered in 1936 and called thiamine (Victor 1984; Kinsella and Riley 1998).

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 surgery 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).

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.

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