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Nutritional peripheral neuropathies
  1. Caroline Kramarz1,
  2. Elaine Murphy2,
  3. Mary M Reilly1,
  4. Alexander M Rossor1
  1. 1 Department of Neuromuscular Diseases, Queen Square UCL Institute of Neurology and National Hospital for Neurology and Neurosurgery, London, UK
  2. 2 Charles Dent Metabolic Unit, The National Hospital for Neurology and Neurosurgery, London, UK
  1. Correspondence to Dr Alexander M Rossor, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK; a.rossor{at}


Nutritional peripheral neuropathies are a global problem, heavily influenced by geopolitical, cultural and socioeconomic factors. Peripheral neuropathy occurs most frequently secondary to B-vitamin deficiencies, which is suspected to increase in years to come due to the popularity of vegan and vegetarian diets and increased use of bariatric surgery.

This review will focus on the common B-vitamins for which a causal link to peripheral neuropathy is more established (vitamins B1, B2, B6, B9 and B12). We will review the historical human and animal data on which much of the clinical descriptions of vitamin deficiencies are based and summarise current available tools for accurately diagnosing a nutritional deficiency. We will also review recently described genetic diseases due to pathogenic variants in genes involved in B-vitamin metabolism that have helped to inform the phenotypes and potential causality of certain B-vitamins in peripheral neuropathy (B2 and B9).

Endemic outbreaks of peripheral neuropathy over the last two centuries have been linked to food shortages and nutritional deficiency. These include outbreaks in Jamaican sugar plantation workers in the nineteenth century (Strachan’s syndrome), World War two prisoners of war, Cuban endemic neuropathy and also Tanzanian endemic optic neuropathy, which remains a significant public health burden today. An improved understanding of lack of which vitamins cause peripheral neuropathy and how to identify specific deficiencies may lead to prevention of significant and irreversible disability in vulnerable populations.


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  • Contributors CK and AMR were involved in the design and conception of the paper. CK wrote the first draft. CK, EM, MMR and AMR edited, critically revised and approved the final manuscript for submission.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests CK is supported by a UCL Queen Square Institute of Neurology and Cleveland Clinic London MPhil/PhD Neuroscience fellowship.

  • Provenance and peer review Commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.