Campbell C H
Contemp Neurol Ser. 1975;12:259-93.
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.
重症肌无力是神经科医生极为关注的课题。然而,蛇咬伤引发的临床表现类似于重症肌无力危象,却很少引起神经科医生的兴趣。这种情况部分是因为大多数蛇咬伤发生在医生(更不用说神经科医生)不常见的地区。因此,很少有神经科医生见过蛇咬伤累及神经系统的病例。这很不幸,因为许多已发表的蛇咬伤病例由于缺乏神经科医生可能提供的详细检查和观察而质量较差。蛇毒中毒的临床表现不仅对神经科医生、血液科医生、心脏病专家和肾脏科医生来说是一个引人入胜的共同临床关注点,而且了解蛇毒作用于神经系统的方式对神经科医生也很重要,因为神经毒性蛇毒主要作用于神经肌肉接头。它们导致随意肌弛缓性麻痹,并因呼吸阻塞和/或呼吸功能不全而致死。就像目前正在作为抗凝剂使用和评估的马来亚蝮蛇(红口蝮)毒液的纯化去纤维蛋白组分(“Arvin”)一样,早在1891年之前,劳特勒就预见到了一种能产生持续两天或更长时间弛缓性麻痹的纯化神经毒素的治疗可能性,他在实验中“将蝰蛇毒……注射到一名患有创伤性破伤风(牙关紧闭)的男孩皮下,使其全身肌肉松弛”。本章将首先描述蛇咬伤累及神经系统的临床表现,特别强调澳大利亚蛇咬伤。描述将基于在莫尔斯比港总医院对56例蛇咬伤后出现麻痹的患者进行的为期七年的观察,以及一些已发表的澳大利亚蛇咬伤病例。然后讨论将涵盖最近一些关于蛇毒作用于神经系统的已发表研究,主要涉及眼镜蛇科毒液。最近有几篇综述描述了所有类型蛇毒的毒性特性和作用。