The effects of snake venoms and their neurotoxins on the nervous system of man and animals.
Myasthenia gravis is a subject of tremendous interest ot neurologists. Snake poisoning, however, which gives rise to a clinical picture resembling a myasthenic crisis, has evoked little interest among neurologists. This state of affairs exists partly because most snake bites occur in areas where physicians, let alone neurologists, are not commonly found. Hence, few neurologists have seen a case of snake bite with nervous system involvement. This is unfortunate, because many of the published cases of snake bite are the poorer for the lack of detailed examination and observations that a neurologist might have provided. Not only is the clinical picture of snake envenomation a fascinating one where the neurologist, haematologist, cardiologist, and renal physician can find a common clinical interest, but an understanding of the way in which snake venoms act on the nervous system is of importance to the neurologist since the neurotoxic snake venoms act principally at the neuromuscular junction. They produce a flaccid paralysis of the voluntary muscles and cause death from respiratory obstruction and/or respiratory insufficiency. Like the purified defibrinating fraction("Arvin") of the venom of the Malayan pit viper (Agkistrodon rehodostoma), which is currently being used and evaluated as an anticoagulant, the thereapeutic possibilities of a purified neurotoxin that could produce a flaccid paralysis lasting two days or more were anticipated well before 1891 by Lauterer, who, as a result of his experiments, "injected viper poison...under the skin of a boy suffering from tentanus treaumaticus (lockjaw) and slackened the muscles of the whole body by it." This chapter will initially describe the clinical picture of nervous system involvement in snake bite, with particular emphasis on Australian snake bite. The description will be based on observations made at the Port Moresby General Hospital over a period of seven years on 56 patients with paralysis following snake bite, and on some published cases of Australian snake bite. The discussion will then cover some of the recent published work on the action of snake venoms on the nervous system, dealing mainly with elapid venoms. There are several recent reviews describing the toxic properties and actions of all types of snake venoms.
D000818:Animals; D000997:Antivenins / Q000627:therapeutic use; D001315:Australia; D001763:Blepharoptosis / Q000139:chemically induced; D006801:Humans; D009045:Motor Endplate / Q000503:physiopathology; D009157:Myasthenia Gravis / Q000139:chemically induced*; D009469:Neuromuscular Junction / Q000503:physiopathology; D003473:Neuromuscular Nondepolarizing Agents / Q000494:pharmacology; D009886:Ophthalmoplegia / Q000139:chemically induced; D010243:Paralysis / Q000139:chemically induced*; D012909:Snake Bites / Q000188:drug therapy / Q000401:mortality* / Q000503:physiopathology; D012910:Snake Venoms / Q000494:pharmacology / Q000506:poisoning*; D012911:Snakes / Q000502:physiology; D014688:Venoms / Q000506:poisoning*
D000997:Antivenins; D003473:Neuromuscular Nondepolarizing Agents; D012910:Snake Venoms; D014688:Venoms