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Arsenical Polyneuropathy Of the neuropathies caused by metallic poisoning, that due to arsenic is particularly well known In cases of chronic poisoning, the neuropathic symptoms develop rather slowly, over a period of several weeks or months, and have the same sensory and motor distribution as the nutritional polyneuropathies Gastrointestinal symptoms, the result of ingestion of arsenic compounds, may precede the polyneuropathy, which is nearly always associated with anemia, jaundice, brownish cutaneous pigmentation, hyperkeratosis of palms and soles, and later with white transverse banding of the nails (Mees lines) The disease is accompanied by an excess of arsenic in the urine and hair Pathologically, this form of arsenical neuropathy is generally categorized as of the dying-back (axonal degeneration) type In patients who survive the ingestion of a single massive dose of arsenic, a more rapidly evolving polyneuropathy may appear after a period of 8 to 21 days as discussed earlier The neuropathy may be preceded by severe gastrointestinal symptoms, renal and hepatic failure, and mental disturbances, convulsions, confusion, and coma ie, arsenical encephalopathy the pathologic basis of which is a brain purpura, or pericapillary hemorrhages Initially, the neuropathy that develops in this setting may resemble GBS, both clinically and electromyographically (partial conduction block, prolonged F responses) Diagnosis and treatment of arsenical poisoning are discussed further in Chap 43 Lead Neuropathy (Plumbism) Lead neuropathy is an uncommon disorder In adults, as a rule, it occurs following chronic exposure to lead paint or fumes (from smelting industries or burning batteries) or from ingestion of liquor distilled in lead pipes Its most characteristic presentation is a predominantly motor mononeuropathy in the distribution of the radial nerves (wrist and nger drop) In a few personally observed patients, this was the main abnormality but there was also a slight sensory loss in the radial territory of the hand Less commonly there is foot drop occurring alone or in combination with weakness of the proximal arm and shoulder girdle muscles As pointed out in Chap 43, lead neuropathy seldom occurs in children, in whom lead poisoning usually results in a devastating encephalopathy Although the neuropathy has been known since ancient times, details of the pathology are still obscure Axonal degeneration with secondary myelin change and swelling and chromatolysis of anterior horn cells has been described Lead accumulates in the nerve and may be toxic to Schwann cells or to endothelial capillary cells, causing edema.

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The diagnosis is established by the history of lead exposure, the predominant and restricted motor involvement, the associated medical ndings (anemia, basophilic stippling of red blood cell precursors in the bone marrow, a lead line along the gingival margins, colicky abdominal pain, and constipation), and the urinary excretion of lead and coproporphyrins Blood lead levels of more than 70 mg/dL are always abnormal In patients with lower levels, doubling of the 24-h urinary lead excretion following an infusion of the chelating agent CaNa2 EDTA indicates a signi cant degree of lead intoxication Coproporphyrin in the urine is abnormal in any amount, but it may also be found in porphyria, alcoholism, iron de ciency, and other disorders as well as in lead intoxication Treatment consists of terminating the exposure to lead and eliminating lead from the bloodstream and the bones as discussed in Chap 43 For this purpose, penicillamine, which is generally safe and can be administered orally, is preferable to dimercaprol [British antilewisite (BAL)] or EDTA Other Metals and Industrial Agents Chronic poisoning with thallium and sometimes with lithium, gold, mercury, and platinum (in the antineoplastic agent cisplatin as discussed further on) may produce a sensorimotor polyneuropathy similar to arsenical polyneuropathy; these intoxications are discussed in Chap 43 and the acute form was addressed earlier in the chapter A predominantly motor neuropathy is known to be induced by occupational exposure to metallic mercury and mercury vapor, but the connection to the mercury content in dental amalgam has little credibility Exposure to manganese, bismuth, antimony, zinc, and copper may give rise to systemic signs of poisoning; some of them affect the central nervous system (CNS), but one cannot be certain that any of them speci cally involves peripheral nerves The devastating encephalopathy of organic mercury toxicity does not, to our knowledge, cause neuropathy As mentioned in Chap 43, a predominantly motor polyneuropathy has been reported as a rare complication of gold therapy for rheumatoid arthritis Most often the cumulative dose of gold had exceeded 1 g, but in a few instances the neuropathy occurred with 05 g Painful distal burning is the initial complaint, and weakness and wasting follow The onset of weakness, although usually insidious, can be abrupt enough to simulate GBS There have been trigeminal, facial, and oculomotor palsies One of the unusual features reported, not shared with most other toxic neuropathies, is a marked rise in CSF protein concentration A distal, symmetrical sensorimotor (predominantly sensory) axonopathy may follow exposure to certain hexacarbon industrial solvents These include n-hexane (found in contact cements, thus affecting glue sniffers who inhale the vapors); methyl n-butyl ketone (used in the production of plastic-coated and color-printed fabrics); dimethylaminopropionitrile (DMAPN), used in the manufacture of polyurethane foam); the fumigant methyl bromide; and the gas sterilant ethylene oxide Operating room nurses may be affected by the latter when the agent is absorbed through the skin, leaving a characteristic rash at exposed sites (usually the wrists, where a surgical gown ends) A mild peripheral neuropathy and CNS changes of memory loss and headaches have been reported by Brashear and colleagues Nurses are also subject to a risk of nitrous oxide neurotoxicity; but at the present time the neuropathy has most often resulted from its repeated use as a euphoriant The process is said to have the clinical and electrophysiologic features of a distal axonopathy but is more likely a myeloneuropathy related to impairment of vitamin B12 metabolism The associated macro-.

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