The authors believe it worth mentioning that there is no convincing evidence linking typical dietary ingestion of fish containing metallic compounds such as mercury and any neurologic or developmental disease. The inhalation of vaporized mercury as a result of extensive dental work, or simply the presence of a large number of fillings (“amalgam illness”), is alleged to affect the peripheral nerves or to cause fatigue, but the connection is also highly doubtful as is the alleged relationship between vaccines containing mercury preservatives (thiomersal) and autism.
Treatment Treatment consists of removal from the source of mercury exposure, and for acute inorganic mercury poisoning, chelation therapy with penicillamine or dimercaprol (BAL). No chelator for methylmercury or ethylmercury is approved by the FDA. In the treatment of chronic mercury poisoning, penicillamine has been the drug of choice, because it can be administered orally and appears to chelate mercury selectively, with less effect on copper, which is an essential element in many metabolic processes.
Nervous system function may be deranged as part of acute and frequently fatal poisoning with inorganic phosphorus compounds (found in rat poisons, roach powders, and match heads). More important clinically is poisoning with organophosphorus compounds, the best known of which is triorthocresyl phosphate (TOCP).
Organophosphates are widely used as insecticides. Since 1945, approximately 15,000 individual compounds in this category have come into use. Certain ones, such as tetraethylpyrophosphate, have been the cause of major outbreaks of neurologic disorder, especially in children. These substances have an acute anticholinesterase effect but no delayed neurotoxic action. Chlorophos, which is a 1-hydroxy-2,2,2-trichlorethylphosphonate, is an exception; it has both an acute and delayed action, as does TOCP.
The immediate anticholinesterase effect manifests itself by headache, vomiting, sweating, abdominal cramps, salivation, wheezing (secondary to bronchial spasm), miosis, and muscular weakness and twitching. Most of these symptoms can be reversed by administration of atropine and pralidoxime. The delayed effect manifests 2 to 5 weeks following acute organophosphorus insecticide poisoning. This takes the form of a distal symmetrical sensorimotor (predominantly motor) polyneuropathy, progressing to muscle atrophy (see Chap. 43). Recovery occurs to a variable degree and then, in patients poisoned with TOCP, signs of corticospinal damage become detectable. The severity of paralysis and its permanence vary with the dosage of TOCP. Whether a polyneuropathy can arise without the preceding symptoms of cholinergic toxicity is debated; however, based on a review of the subject and a study of 11 patients exposed to these agents, 3 of whom later acquired sensory neuropathy, Moretto and Lotti express the view that such an occurrence must be rare.
In addition to the acute and delayed neurotoxic effects of organophosphorus, an intermediate syndrome has been described (Senanayake and Karalliedde). Symptoms appear 24 to 96 h after the acute cholinergic phase and consist of weakness or paralysis of proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles. Respiratory paralysis may prove fatal. In patients who survive, the paralytic symptoms last for 2 to 3 weeks and then subside. The intermediate and delayed symptoms do not respond to atropine or other drugs.