The therapeutic injection of small quantities of botulinum toxin into a muscle affected by dystonia or spasticity will weaken it for weeks to months (see Chap. 4). Mild symptoms of botulism can occur with relatively large therapeutic doses, mainly affecting the oropharyngeal and ciliary muscles, and was more common a few decades ago when experience was limited. Cases are seen after “botox parties” or illicit non-physician use.
PLANT POISONS, VENOMS, BITES,
Ergotism is the name applied to poisoning with ergot, a drug derived from the rye fungus Claviceps purpurea. Ergot is used therapeutically to control postpartum hemorrhage caused by uterine atony; one of its alkaloids, ergotamine, is used in the treatment of migraine (see Chap. 9), and a class of dopamine agonists, now less used in the treatment of Parkinson disease, has ergot activity (see Chap. 38). Chronic and repeated use of the drug is the usual cause.
Two types of ergotism are recognized: gangrenous, which is caused by a vasospastic, occlusive process in the small arteries of the extremities, and convulsive, or neurogenic, ergotism. The latter is characterized by fasciculations, myoclonus, and spasms of muscles, followed by seizures. In nonfatal cases, a tabes-like neurologic syndrome may develop, with loss of knee and ankle jerks, ataxia, and impairment of deep and superficial sensation. The pathologic changes consist of degeneration of the posterior columns, dorsal roots, and peripheral nerves, but they have been poorly described. The relation of these changes to ergot poisoning is not clear, because most of the cases occurred in areas where malnutrition was endemic.
Lathyrism is a neurologic syndrome characterized by the relatively acute onset of pain, paresthesia, and weakness in the lower extremities, progressing to a permanent spastic paraplegia. It is a serious medical problem in India and in some North African countries and is probably caused by a toxin contained in the chickling vetch pea, Lathyrus, a legume that is consumed in excess quantities during periods of famine. This disorder is discussed further with the spinal cord diseases (see Chap. 42).
Konzo (Environmental Cyanide Poisoning.
See Also Chap. 44)
This is caused by ingestion of cyanide, usually from insufficiently processed roots of the bitter cassava. The illness is a rapid upper motor syndrome (paraplegia, tetrapelgia) and usually irreversible. It is most common in rural Africa and peaks in incidence during times of food shortage and drought, when cassava is utilized as a food substitute and there is insufficient water to allow for adequate processing of the roots. Efforts are directed towards education and providing resources for processing.
The gathering of wild mushrooms, a popular pastime in late summer and early fall, always carries with it the danger of poisoning. As many as 100 species of mushrooms are poisonous. Most of them cause only transient gastrointestinal symptoms but some elaborate toxins that can be fatal. The most important of these toxins are the cyclopeptides, which are contained in several species of Amanita phalloides and muscaria and account for more than 90 percent of fatal mushroom poisonings. These toxins disrupt RNA metabolism, causing hepatic and renal necrosis. Symptoms of poisoning with Amanita usually appear between 10 and 14 h after ingestion and consist of nausea, vomiting, colicky pain, and diarrhea, followed by irritability, restlessness, ataxia, hallucinations, convulsions, and coma. The important clinical features have been reviewed by Koppel.
There may be added evidence of a neuromyopathy presenting as flaccid areflexic paralysis, high serum CK, diminished EMG potentials, and fiber necrosis.