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  • Updated 01.14.2020
  • Released 11.02.1999
  • Expires For CME 01.14.2023

Nutrition-related peripheral neuropathies

Introduction

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 (68; 33).

Nutritional neuropathies are usually slowly progressive; however, there are situations in which the onset of the neuropathic symptoms may be acute or subacute (69). Alcoholic neuropathy may deteriorate suddenly in a Guillain-Barré-like fashion (71). 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 (16; 17). Following gastric surgery for weight loss, individuals may develop a severe debilitating axonal neuropathy within weeks following unremitting vomiting (57; 15; 56; 63; 23). Large doses of pyridoxine (2000 mg every day or even lesser amounts) can precipitate an acute sensory neuropathy over several weeks (61).

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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