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[滥用氧化亚氮后亚急性脊髓神经病:周围神经的电子显微镜研究]

[Subacute myeloneuropathy after abuse of nitrous oxide: an electron microscopic study on the peripheral nerve].

作者信息

Shimizu T, Nishimura Y, Fujishima Y, Miyajima H, Honda N

出版信息

Rinsho Shinkeigaku. 1989 Sep;29(9):1129-35.

PMID:2557181
Abstract

We have experienced a case of myeloneuropathy following habitual abuse of nitrous oxide. We report clinical and pathological findings of this case with review of literatures. A 36-year-old dentist was first admitted to our hospital on August 17, 1983 because of numbness of both lower legs and unsteady gait. He had recreationally inhaled nitrous oxide 30 to 60 minutes everyday since a year ago. Neurological examination showed ataxic broad-based gait, moderate loss of pain and touch sensation in the lower limbs up to patella. Position and vibratory senses were more severely impaired. Deep tendon reflexes increased in the upper extremities and at the knees, but diminished at ankle jerks. Muscle strength was normal. Prominent Lhermitte's sign was present. Except for reduced serum vitamin B12 level, laboratory results were normal. Needle electromyography showed high amplitude and long duration NMU in the right quadriceps and anterior tibial muscles. Motor nerve conduction velocity was 34 m/sec at the right posterior tibial nerve and could not be detected at the left. Sural nerve biopsy was performed. The density of the myelinated fibre measured on transverse section was in normal range but degenerated fibres were occasionally recognized. Single teased nerve fibre showed various degree of myelin ovoid along the fibre. Myelin loss was shown to occur in some parts of the fibre. Electron microscopy showed myelin splitting and formation of intramyelinic vacuoles containing myelin debris. Axon was almost normal at least in the early stage of degeneration. Later, axon disappeared with destruction of myelin sheath. These nerve changes largely demonstrated demyelination but it was occasionally accompanied with axonal degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们遇到了一例因习惯性滥用氧化亚氮导致的脊髓神经病病例。我们报告该病例的临床和病理 findings,并复习相关文献。一名36岁的牙医于1983年8月17日首次因双下肢麻木和步态不稳入住我院。自一年前起,他每天有30至60分钟用于消遣性吸入氧化亚氮。神经系统检查显示宽基底共济失调步态,下肢直至髌骨处疼痛和触觉中度丧失。位置觉和振动觉受损更严重。上肢和膝部的深腱反射增强,但踝反射减弱。肌力正常。有明显的莱尔米特征。除血清维生素B12水平降低外,实验室检查结果均正常。针极肌电图显示右股四头肌和胫前肌运动单位电位(MNU)波幅增高、时限增宽。右胫后神经运动神经传导速度为34米/秒,左侧未测出。进行了腓肠神经活检。横切面上测量的有髓纤维密度在正常范围内,但偶尔可识别出变性纤维。单根分离神经纤维显示沿纤维有不同程度的髓鞘卵圆体。纤维的某些部位出现髓鞘脱失。电子显微镜显示髓鞘分裂和形成含有髓鞘碎片的髓鞘内空泡。轴突至少在变性早期基本正常。后来,随着髓鞘破坏轴突消失。这些神经改变主要表现为脱髓鞘,但偶尔伴有轴索性变性。(摘要截短至250字)

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