Bleck T P, Jacobsen J
Department of Neurology, University of Virginia School of Medicine, Charlottesville.
Clin Neuropharmacol. 1991 Oct;14(5):457-62. doi: 10.1097/00002826-199110000-00011.
A 23-year-old man with a lymphoblastic lymphoma accidentally received 2.0 mg of vincristine intrathecally instead of intravenously. Although he underwent immediate CSF drainage, symptoms of an ascending myeloencephalopathy developed at 48 h. This progressed to coma, initially with a diffusely slow EEG, which evolved into alpha coma. He also developed a left frontal focus of epileptiform activity. He was transferred to our institution 1 month later. His court-appointed guardian refused to allow discontinuation of supportive treatment; therefore, the evolution of the disorder can be followed for 12 months. Although alpha coma remained the predominant pattern, some EEG evolution did occur, with a progressive decrease in amplitude being most prominent. An increase in amplitude in the 10th month was accompanied by the return of some nystagmoid eye movements. The patient's lymphoma then recurred, and further treatment was not attempted. This tragic case, in which transient exposure to a microtubular poison produced severe CNS toxicity, allows some insights into the mechanisms of alpha coma.
一名23岁的淋巴细胞性淋巴瘤患者意外鞘内注射了2.0毫克长春新碱而非静脉注射。尽管他立即接受了脑脊液引流,但48小时后出现了上升性脊髓脑病症状。病情进展为昏迷,最初脑电图广泛减慢,随后演变为α昏迷。他还出现了左侧额叶癫痫样活动灶。1个月后他被转至我院。他的法庭指定监护人拒绝停止支持治疗;因此,可以对该疾病的进展进行12个月的跟踪观察。尽管α昏迷仍是主要模式,但脑电图确实发生了一些变化,其中最显著的是波幅逐渐降低。第10个月波幅增加的同时,出现了一些眼球震颤样眼动。随后患者淋巴瘤复发,未再尝试进一步治疗。这个悲剧性病例中,短暂接触微管毒物导致了严重的中枢神经系统毒性,有助于深入了解α昏迷的机制。