ARSENIC
Arsenic has a ubiquitous distribution in the environment, particularly as an impurity in copper ores. Although it is a means of notorious surreptitious homicide, the presence of excessive levels of arsenic in a patient should not immediately indicate a possible criminal cause. Arsenic contamination may be due to exposure to an agricultural environment or to an industrial environment, such as copper smelting. Other sources have included drinking water (e.g., when a well has been inadvertently drilled in a former storage location of arsenic insecticides). The clinical manifestations of arsenic poisoning may vary. Usually, the initial symptoms are gastrointestinal rather than neuropathic, and vomiting, diarrhea, and abdominal pain are common early signs of poisoning. The peripheral nerve manifestations ultimately follow, usually as length-dependent sensory symptoms with a prominent pain component, followed by weakness. These symptoms may continue to progress for a period of time after the source of exposure is gone. Central nervous system findings are often present, such as confusion and psychiatric symptoms. Skin changes may eventually occur with erythema or abnormal areas of pigmentation. Occasionally, if the amount ingested is sufficiently large, growth-arrest lines, so-called Mees lines, may be seen in the fingernails. The diagnosis is confirmed by analysis of a 24-hour urine sample, a more sensitive indicator than serum values, which can decrease rapidly after exposure has ceased. Differentiation between inorganic and organic arsenic is important, because some dietary sources (e.g., seafood) can result in elevations of urinary arsenic in a nontoxic form. Samples of hair and nails may provide supporting evidence of arsenic exposure, and may be useful to analyze long after the exposure has ceased. If electrophysiologic tests are performed, they will generally show an axonal peripheral neuropathy. The most important treatment components are removing the source of the arsenic and use of chelating agents.
NEUROPATHIES CAUSED BY OTHER METALS
Gold salts, which had been used in treating rheumatoid arthritis, have sometimes produced a distal sensorimotor peripheral neuropathy, although sometimes this can be difficult to separate clinically from neuropathy secondary to rheumatoid arthritis itself. Improvement in neuropathic symptoms after discontinuation of gold salts usually confirms an underlying toxic mechanism. Ingestion of thallium salts, occasionally used in rodenticides and insecticides, causes a potentially severe sensorimotor neuropathy associated with development of alopecia 10 to 30 days after ingestion. Exposure to lead, now seen infrequently, can cause a predominantly motor neuropathy, often initially involving wrist and finger extensors

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