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  • Updated 04.01.2024
  • Released 09.21.1999
  • Expires For CME 04.01.2027

Toxic peripheral neuropathies



In this article, the authors discuss general principles regarding toxic peripheral neuropathy. This clinical entity is most commonly encountered as an adverse effect of medications, but environmental and occupational exposure can also result in toxic neuropathy. The authors give clues to help guide the process of evaluation in patients suspected of having toxic peripheral neuropathy.

Key points

• Toxic neuropathy should have a temporal and dose-response relationship between symptoms and exposure.

• There should be consistency of disease in those with similar exposures.

• Improvement (or at least stabilization) of neuropathic symptoms should occur when exposure ceases.

Historical note and terminology

Despite widespread media attention to their rare epidemic occurrence, toxic polyneuropathies are relatively infrequent in North America. Neurotoxic exposure may be due to: (1) pharmaceutical agents, either self or iatrogenically administered; (2) chemical exposure in the workplace; (3) environmental chemical exposure at home or elsewhere; or (4) intoxications due to suicide, recreational abuse, or homicide. Most toxic polyneuropathies encountered in routine clinical practice are due to iatrogenic pharmaceutical intoxications; epidemic occupational exposure, as with large pharmaceutical companies, receives the media headlines but is unusual. The majority (and unfortunately the most difficult) of the cases of toxic polyneuropathies are individual intoxications due to small-scale, often chance, occupational exposure, and also due to intentional, suicidal ingestion. The exception to the above rule involves reports of endemic arsenic exposure due to ground water contamination in West Bengal, India (09), and Taiwan.

The determination that a sporadic peripheral neuropathy has resulted from toxin exposure in the occupational setting is often made difficult by an unclear exposure history. Toxic polyneuropathies are usually distal axonopathies that clinically and electrophysiologically resemble neuropathies from metabolic abnormalities, nutritional deficiencies, or systemic illnesses. Clinically relevant and reliable toxicological tests are often not helpful, either because the necessary laboratory tests are not available or because the substance is undetectable due to the delay between exposure and examination. Consequently, when a naturally occurring medical cause is not readily apparent, there is an unfortunate tendency for many peripheral neuropathies to be misdiagnosed as toxic in nature.

Our limited knowledge of the biochemical and pathophysiologic mechanisms of most neurotoxins has led to a simplistic classification system according to compound class (eg, solvents, metals). Such a classification is clinically of little help and potentially misleading. A compound cannot be presumed to be neurotoxic because of a superficial resemblance to a related known toxin of similar class; not all compounds within the same class are neurotoxic (eg, acrylamide monomer is capable of producing a devastating peripheral neuropathy, whereas the polymer is innocuous). Structure-toxicity relationships are clear for only a few classes of substances, such as organophosphates and hydrocarbons.

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