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Review
Toxic neuropathies: a practical approach
  1. Duncan Smyth,
  2. Caroline Kramarz,
  3. Aisling S Carr,
  4. Alexander M Rossor,
  5. Michael P Lunn
  1. MRC Centre for Neuromuscular Diseases, National Hospital for Neurology and Neurosurgery, London, UK
  1. Correspondence to Dr Duncan Smyth, MRC Centre for Neuromuscular Diseases, National Hospital for Neurology and Neurosurgery, London, WC1N 3BG, UK; duncan.smyth{at}nhs.net

Abstract

Toxic neuropathies result from exogenous substances damaging the peripheral nerves. There are numerous causes, including prescribed and recreational drugs, heavy metals, industrial agents and biological toxins. Timely recognition of these neuropathies gives better outcomes, as they usually improve or stabilise once the toxin is removed. Most toxic neuropathies are axonal, length-dependent and sensory predominant, although some have significant motor involvement or can present acutely or subacutely. Here, we outline our clinical approach and discuss the major causes of toxic neuropathy, while emphasising the clinical and neurophysiological features and the neuropathy phenotype. We also include an update on newer medications that can cause neuropathy, including immune checkpoint inhibitors and BRAF/MEK inhibitors.

  • NEUROPATHY
  • NEUROONCOLOGY
  • NEUROPHYSIOLOGY
  • NEUROTOXICOLOGY
  • CLINICAL NEUROLOGY

Data availability statement

Data sharing not applicable as no datasets generated and/or analysed for this study.

http://dx.doi.org/10.1136/pn-2022-003444

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    Data availability statement

    Data sharing not applicable as no datasets generated and/or analysed for this study.

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    Footnotes

    • Twitter @duncansmyth, @mike_the_nerve

    • Contributors DS and MPL were involved in the design and conception of the paper. DS and CK wrote the first draft. DS, CK, ASC, AMR and MPL 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 DS is supported by the New Zealand Neurological Foundation. CK is supported by a UCL Queen Square Institute of Neurology and Cleveland Clinic London MPhil/PhD Neuroscience fellowship. ASC, AMR and MPL are supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. DS, CK, ASC, AMR and MPL received no funding or sponsorship for this commissioned paper. ASC has received honoraria from CSL, Grifols, Akcea, BMS, BeiGene and Lupin for educational talks and advisory input. MPL has provided consultancy for UCB Pharma, CSL Behring and Polyneuron. He was the principal investigator on trials with Polyneuron and UCB Pharma for which his institution receives investigator fees. He has been on the data safety monitoring board for Octapharma, IoC trial, AstraZeneca Pharmaceuticals.

    • Provenance and peer review Commissioned; externally reviewed by Tim Lavin, Manchester, UK.

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