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“Poison is in everything, and nothing is without poison. The dosage makes it either a poison or a remedy.”

Paracelsus (1493–1541)

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Objectives

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On completion of this chapter, the student/practitioner will be able to:

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  • Identify common environmental toxins and exposure vectors that may lead to peripheral neuropathy.

  • Discuss the type of neuropathy associated with each toxin and the common clinical picture including signs and symptoms that may be encountered by rehabilitation therapists.

  • Construct treatment intervention schema for each of the common environmental toxic neuropathies presented.

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Key Terms

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  • Alcohol

  • Arsenic

  • Lead

  • Mercury

  • Nitrous oxide

  • Thallium

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Introduction

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Knowledge of the neurotoxicity of environmental compounds and elements has a very practical application in the evaluation of patients with signs and symptoms of peripheral neuropathy. Consultation on patients with numerous neurotoxic exposures including environmental compounds and elements; prescribed, over-the-counter, and recreational drugs; and dietary and absorption compromises is common.

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Exposure often is occupational or related to a hobby, but occasionally there is exposure by happenstance or, especially in cases of nitrous oxide, thallium, and ethylene glycol, purposeful exposure. These compounds and elements produce signs and symptoms common to neuropathies associated with medication, primary or secondary disease processes, and biomechanical forces. An astute clinician is able to identify the etiological agent through careful history-taking, follow-up questioning, laboratory data analysis, and a valid and reliable physical examination.

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For example, nitrous oxide, a potent etiological agent for peripheral neuropathy, is commonly found in the aerospace, automobile, and food preparation industries. It is also used as a dental anesthetic. Additionally, nitrous oxide is a popular recreational drug. Ethylene glycol is a very common toxin because of its use as a coolant in automobiles. Metal toxicity (thallium, arsenic, and lead) receives much commentary in neurological and pathophysiology textbooks and is of interest to medical practitioners when investigating the etiology of peripheral neuropathy. The etiology of alcohol neuropathy is most likely twofold: (1) a nutritionally based neuropathy primarily owing to thiamine deficiency and (2) the direct toxic effects of alcohol on the peripheral nerve.

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In this chapter, we discuss the relationship of the exposure of specific common environmental compounds and elements and the onset and pathogenesis of peripheral neuropathy. Toxins are discussed under specific headings as follows: anesthetic agent, heavy metal toxicities, and chemical toxicities including alcohol-related neuropathy. There are hundreds of environmentally and clinically available toxins that, with exposure, may lead to symptoms of peripheral neuropathy. It is beyond the scope of this book to include all of these toxins. Chapter 11 discusses medication-associated neuropathy.

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Anesthetic Agent

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Nitrous Oxide

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Nitrous oxide (N2O) is more commonly known to the lay population as “laughing gas.” It is a nonflammable, inorganic gas used in medicine, in industry, and as a recreational drug. ...

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