Treatment consists of terminating the exposure to lead and eliminating lead from the bloodstream and the bones by chelation as discussed in Chap. 41. For this purpose, penicillamine, which is generally safe and can be administered orally, is preferable to dimercaprol (British anti-Lewisite [BAL]) or EDTA.
Chronic poisoning with thallium and sometimes with lithium, gold, mercury, and platinum (in the antineoplastic agents cisplatin and carboplatin as discussed further on) produces a sensorimotor polyneuropathy; these intoxications are discussed in Chap. 41 and the acute form was addressed earlier in the chapter. A predominantly motor neuropathy is induced by occupational exposure to metallic mercury and mercury vapor but any 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 specifically involves peripheral nerves. The devastating encephalopathy of organic mercury toxicity does not, to our knowledge, cause neuropathy.
As mentioned in Chap. 41, 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 0.5 g. Painful distal burning is the initial complaint with weakness and wasting following. 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, not shared with most other toxic neuropathies, is a marked rise in CSF protein concentration.
A distal, symmetrical sensorimotor (predominantly sensory) neuronopathy may follow exposure to certain hexacarbon industrial solvents. These include n-hexane (found in contact cements, thus affecting individuals 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 from this agent by Brashear and colleagues. Nurses are also subject to a risk of nitrous oxide neurotoxicity and this usually takes the form of a myelopathy similar to that seen with cobalamin deficiency. Most cases are caused by repeated use of the gas to induce euphoria. As with vitamin B12 deficiency, the syndrome may be mistaken for a neuropathy but nerve conduction studies fail to demonstrate one. The associated macrocytic anemia is reversed by the administration of B12, but the neurologic illness may be less responsive as discussed in Chap. 40. Whether folate deficiency, sometimes in the context of alcohol excess, and mostly in countries without folate fortification programs, causes polyneuropathy has been a matter of debate. A series by Koike and colleagues describes a mundane, sensory-predominant neuropathy.