Several striking outbreaks of TOCP poisoning have been reported. During the latter part of the prohibition era and to a lesser extent thereafter, outbreaks of so-called jake paralysis were traced to drinking an extract of Jamaica ginger that had been contaminated with TOCP. Adams had examined several “ginger jake” patients many years later and related to us that he found only signs of corticospinal disease. Presumably in the early stage of this disease they were obscured by the neuropathy. Another outbreak occurred in Morocco in 1959, when lubricating oil containing TOCP was used deliberately to dilute olive oil. Several other outbreaks have been caused by the ingestion of grain and cooking oil that had been stored in inadequately cleaned containers previously used for storing TOCP.
The effect of TOCP on the peripheral nervous system has been studied extensively in experimental animals. In cats, there occurs a dying back from the terminal ends of the largest and longest medullated motor nerve fibers, including those from the annulospiral endings of the muscle spindles (Cavanagh and Patangia). The long fiber tracts of the spinal cord show a similar dying-back phenomenon. Abnormal membrane-bound vesicles and tubules were observed by Prineas to accumulate in axoplasm before degeneration. These effects have been traced to the inhibitory action of TOCP on esterases. There is still uncertainty as to the details of these reactions, and no treatment for the prevention or control of the neurotoxic effects has been devised.
In the late nineteenth century, thallium was used medicinally in the treatment of venereal disease, ringworm, and tuberculosis, and later in rodenticides and insecticides. Poisoning was fairly common. Sporadic instances of poisoning still occur, usually as a result of accidental or suicidal ingestion of thallium-containing rodenticides and rarely from overuse of thallium-containing depilatory agents. Patients who survive the effects of acute poisoning develop a rapidly progressive and painful sensory polyneuropathy, optic atrophy, and occasionally ophthalmoplegia—followed, 15 to 30 days after ingestion, by diffuse alopecia (see Chap. 43). The latter feature should always suggest the diagnosis of thallium poisoning, which can be confirmed by finding this metallic element in the urine. The main clinical features have been reviewed by Bank et al. Two of our patients with thallium poisoning had a severe sensory and mild motor polyneuropathy and alopecia, from which they were recovering months later. It is not uncommon for the neuropathy to have a painful component involving acral regions. The condition can end fatally. The use of potassium chloride by mouth may hasten thallium excretion.
Iron, antimony, tin, aluminum, zinc, barium, bismuth, copper, silver, gold, platinum, and lithium may all produce serious degrees of intoxication. The major manifestations in each case are gastrointestinal or renal, but certain neurologic symptoms—notably headache, irritability, confusional psychosis, stupor, coma, and convulsions—may be observed in any of these if the poisoning is severe, often as a terminal event.
Gold preparations, which are still used occasionally in the treatment of arthritis, may, after several months of treatment, give rise to focal or generalized myokymia and a rapidly progressive, symmetrical polyneuropathy (Katrak et al). The adverse effects of platinum are discussed later, with the antineoplastic agents. Lithium was discussed earlier.
Mentioned here is a novel but quite rare cobalt-chromium metallosis due to the leaching of metals from prosthetic hips into surrounding tissues. A painful sensorimotor polyneuropathy has been reported, in some patients accompanied by hearing loss. Although only a few cases have been documented, the process has attracted considerable attention and our only encounter with it has been the ill-advised revision of hip implants for nondescript sensory symptoms, similar to the peculiar obsession with removing dental fillings for erroneously diagnosed mercury poisoning.